SYNOPSIS    OF    LECTURES 


Diseases  of  ttie  Nervous  System, 


DELIVERED    AT    THE 


COLLEGE  OF  PHYSICL^NS  AND  SURGEONS, 

MEDICAL  DEPARTMENT  OF  COLUMBL\  UNIVERSITY, 

NEW  YORK. 


BY 

M.   ALLEN  STARR,   M.D.,   Ph.D.,   LL.D., 
Professor  of  Neurology. 


New  York:   . 
James  T.   Dougherty,   Publisher, 

409  &  411  West  Fifty-ninth  Street. 


COPYBIGHT,    1904, 

BY 

JAMES    T.    DOUGHERTY. 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/synopsisoflectuOOstar 


SYNOPSIS  OF  LECTURES 

UPON 

DISEASES  OF  THE  MERYOUS  SYSTEM. 


A  KNOWLEDGE  of  the  Structure  and  functions  of  the  central 
nervous  system  is  an  essential  preliminary  to  the  study  of  its 
diseases.  The  human  nervous  system  is  the  most  complex  of  all 
nervous  structures,  and  is  the  culmination  of  the  process  of  evolu- 
tion. It  will  aid  in  the  understanding  of  its  structure  if  the 
various  stages  in  its  evolution  are  known. 

The  Evolution  of  the  Nervous  System. 

The  simplest  form  of  a  nervous  system  consists  of  a  single 
mass  of  gray  matter  with  a  sensory  and  a  motor  nerve. 

The  mass  of  gray  matter  receives  impulses  sent  from  the 
surface  by  the  sensory  fibre,  acts  in  response  to  the  impulse,  and 
the  action  is  transmitted  to  a  motor  mechanism  by  the  motor 
nerve. 

Example.  The  closure  of  an  oyster-shell  when  the  oyster 
feels  any  object  touching  its  sensory  surface.  Parallel  action  in 
human  system — any  spinal  reflex — e.g.,  knee-jerk. 

Several  such  single  masses  may  be  joined  to  one  another, 
each  with  its  sensory  and  motor  nerve.  The  masses  receive  im- 
pulses in  succession  and  act  in  succession. 

Example.     Wave-like  motion  of  a  jelly-fish  or  caterpillar. 

A  compound  type  of  nervous  system  consists  of  several  sub- 
ordinate masses  joined  together  and  presided  over  by  a  single 
higher  mass,  which  is  joined  to  each  of  the  lower  masses.  The 
higher  mass  receives  impulses  from  the  lower  masses,  not  directly 
from  the  surface.  It  sends  impulses  to  the  motor  mechanisms 
through  the  lower  masses,  not  directly.  It  secures  a  certain  defin- 
ite succession  and  combination  of  action  in  the  lower  masses. 


4  DISEASES    OF    THE    NERVOUS    SYSTEM. 

Examples.  The  nervous  system  of  a  frog  experimentally  de- 
prived of  its  hemispheres,  capable  of  automatic  acts  of  swim- 
ming-. The  automatic  act  of  respiration  in  man.  In  man  the 
facial,  laryngeal,  intercostal,  thoracic,  and  diaphragmatic  re- 
spiratory muscles  act  in  definite  succession  and  rhythm  in  the 
act  of  breathing;  and  this  act  is  presided  over  by  a  single  centre 
in  the  medulla  controlling  the  lower  medullary  and  spinal  centres. 

The  higlicst  type  of  nervous  system  is  the  complex  type. 
There  are  the  lower  centres  as  in  the  sim/ple  type.  There  are 
higher  centres  controlling  the  lower  centres,  as  in  the  compound 
type.     There  is  a  supreme  mass  controlling  both  the  others. 

This  is  the  form  found  in  all  vertebrates,  and  the  degree 
of  evolution  in  the  highest  or  supreme  mass  determines  the  place 
of  the  animal  in  the  scale  of  intelligence. 

In  man  the  supreme  mass  is  the  cerebral  cortex,  the  next 
lower  or  automatic  centres  are  the  optic  thalami  and  corpora  stri- 
ata, including  gray  masses  in  the  cerebral  axis ;  the  lowest  or 
reflex  centres  are  the  cranial  nerve  nuclei  in  the  cerebral  axis 
and  the  gray  matter  of  the  spinal-cord  segments. 

These  distinct  gray  masses  are  joined  with  one  another  in  all 
possible  combinations  by  means  of  the  white  nerve  tracts,  which 
pass  in  all  directions  around  and  within  them. 

Read  Herbert  Spencer,  '  Principles  of  Psychology,"  Part  I.,  Chaps.  I. -IV. 
Charles  Mercier,  "The  Nervous  System  and  the  Mind,"  Part  I. 

The  Neurone. 

The  primary  elements  of  the  nervous  system  are  neurones, 
and  the  nervous  system  from  the  simplest  to  the  most  complex  in 
the  order  of  evolution  consists  of  a  collection  of  such  neurones  of 
greater  or  lesser    complexity. 

The  neurone  consists  of : 

(ist)  A  cell  body  whose  shape  and  size  vary  at  different 
parts  of  the  nervous  system. 

(2d)  Dendrites  or  protoplasmic  prolongations  of  the  cell 
body  which  divide  and  subdivide  as  they  extend  outward  from  it 
much  like  the  roots  of  a  tree.  The  surface  of  these  dendrites  is 
rough,  appearing  like  moss  under  the  microscope  on  account  of  the 


DISEASES    OF    THE    xXERVOUS    SYSTEM.  5 

presence  of  fine  granules.  Nervous  impluses  are  collected  by 
these  dendrites  and  transmitted  to  the  cell  body.  Fine  filaments 
have  been  demonstrated  passing  from  each  dendrite  through  the 
cell  body  and  entering  the  axon. 

.  (3d)  The  axon  or  axis-cylinder  process  of  the  cell  body  is  a 
single  long,  projecting  fibre  passing  outward  from  the  cell  body 
and  transmitting  impulses  from  the  cell  body  to  a  distance.  The 
neuraxon  gives  ofif  fine  collateral  branches  in  its  course  and 
terminates  as  do  its  collaterals  in  a  fine  brush-like  end.  This 
brush  is  supposed  to  come  in  contact  with  the  gemmules  of  the 
dendrites  of  other  neurones  so  that  connection  between  different 
neurones  is  possible.  The  axon  is  made  up  of  many  fine  fibrillje 
which,  as  already  stated,  have  come  through  the  cell  from  the 
dendrites.  The  cell  body  controls  nutrition  of  the  dendrites  and 
axon  so  that  when  it  is  destroyed  they  atrophy.  Golgi  divides 
neurones  into  two  types.  In  the  first  type  the  axon  extends  to  a 
distance  and  ends  in  a  single  brush.  In  the  second  type  the  axon 
divide  into  numerous  branches  near  the  cell  body  and  ends  in  a 
network  of  fibres. 

Tlie  Structure  of  a  Neurouc. — A  fine  trabeculum  or  frame- 
work appears  to  be  filled  with  semifluid  protoplasm,  which  proto- 
plasm is  used  up  by  action  of  the  neurone,  thus  leading  to  altera- 
tions in  size  in  accordance  with  the  amount  of  work  performed. 
The  normal  cell  body  shows  under  straining  with  meth}l  blue  a 
granular  appearance,  and  these  granules  are  termed  chlorophyl 
bodies  and  appear  to  have  a -regular  arrangement  within  the  cell. 
The  protoplasm  within  the  trabeculse  does  not  stain.  In  a  de- 
generated cell  marked  changes  in  the  staining  capacity  and  an 
irregularity  of  arrangement  of  the  chlorophyl  bodies  are  noticed. 

J^aricties  of  Neurones. — Neurones  have  been  divided  accord- 
ing to  their  function  into  :  (ist)  Centrifugal,  which  are  either 
(a)  motor,  (b)  secreting^  (c)  trophic.  (2d)  Centripetal,  or 
sensory.  (3d)  Intrinsic,  or  association.  Neurones  have  also 
been  divided  into  a  series  according  to  their  position,  into  (i) 
primary  neurones  whose  cell  body  lies  in  the  central  nervous 
system  or  in  the  ganglia,  and  whose  axon  extends  thence  to  some 
peripheral  portion  of  the  body,  e.g.,  to  a  muscle,  to  a  gland,  to 


6  DISEASES    OF    'l"HE    NERVOUS    SYSTEM. 

the  skin;  (2)  secondary  neurones  whose  body  Hes  in  the  central 
nervous  organs  and  whose  axon  extends  thence  to  some  other 
part  of  the  central  nervous  organs  to  terminate  about  a  primary 
neurone.  These  neurones  may  lie  in  the  cortex  and  brain  or  in 
the  basal  ganglia  or  medulla. 

All  simple  reflex  acts  involve  the  transmission  of  impulses 
through  primary  neurones  only. 

All  transmission  of  voluntary  motor  impulses,  or  conscious 
sensory  impulses,  involves  the  action  of  both  primary  and  sec- 
ondary neurones. 

The  human  nervous  system  has  two  distinct  portions:  (i) 
the  cerebro-spinal  sy.'^tem,  and  (2)  the  sympathetic  nervous  sys- 
tem. 

( i)  The  cerebro-spinal  system  includes:  (o)  a  peripheral 
portion,  comprising  the  nerves,  (b)  a  central  system,  comprising: 
(i)  the  spinal  cord  and  cranial  nerve  nuceli ;  (ii)  the  cerebellum 
gray  masses  of  the  medulla,  pons,  crura  cerebri,  corpora  quadri- 
gemina,  optic  thalami  and  corpora  striata;  (iii)  the  cerebral 
cortex. 

(2)  The  sympathetic  nervous  system  is  subdivided  into: 
(a)  Two  great  cords  containing  ganglia,  which  lie  on  the  sides 
of  the  vertebral  column  and  are  joined  to  the  spinal  cord  on  one 
side  and  to  the  plexuses  on  the  other;  (b)  Three  pervertebral 
plexuses,  the  cardiac,  solar,  and  hypogastric,  which  are  masses 
of  ganglia  connected  with  the  viscera;  (c)  ]\lany  peripheral 
plexuses  connected  with  various  organs;  (d)  Terminal  mono- 
cellular ganglia  scattered  through  the  viscera;  (e)  Sympathetic 
nerve-fibres  joining  the  plexuses  and  ganglia  together  and  con- 
necting them  with  the  cerebro-spinal  system. 


THE  PERIPHERAL  NERVES  AND  THEIR  DISEASES. 


Structure  of  the  nerves.  Bundles  of  nerve-fibres — large  or 
small. 

Structure  of  a  nerve-fibre:  i.  Axis  cylinder,  a  long  process 
of  some  nerve-cell.  2.  Medullary  sheath  of  myelin — a  fatty  in- 
sulator,, interrupted  at  the  nodes  of  Ranvier.  3.  Connective-tis- 
sue sheath  of  Schwann,  with  its  nucleus.  Nerve-fibres  are  bound 
into  bundles  by  connective  tissue ;  endoneurium,  perineurium. 
The  sympathetic  nerve-fibres  have  no  medullary  sheath. 


Fig.  1.— a  Normal  Nerve, 

All  nerve-fibres  branch  during  their  course  in  the  central 
nervous  system,  sending  out  "collaterals,"  but  do  not  branch  in 
their  peripheral  course.  They  arise  from  a  nerve-cell.  They  ter- 
minate in  fine  brush-like  expansions  which  are  spread  out  in  the 
skin,  or  on  a  muscle,  or  around  another  nerve-cell. 

Nerves  are  divided  into  motor  nerves  and  sensory  nerves, 
according  to  the  mechanism  to  which  they  are  attached.  Motor 
nerves  convey  impulses  outward,  sensory  inward.  Motor  nerves 
grow  outward  from  large  nerve-cells  in  the  spinal  cord.  Sensory 
nerves  grow  from  cells  in  the  posterior  spinal  ganglia,  which  send 
one  branch  to  the  surface,  and  the  other  into  the  spinal  cord. 


Neuritis. 

Neuritis  may  occur  in  a  single  nerve,  or  in  a  plexus. 
Causes. — Injuries,  strains,  pressure,  compression  in  fractures, 
rheumatism,  gout,  cold. 

Pathologw — I.   Parenchymatous  neuritis,  congestion  and  exu- 


8  DISEASES    OF   THE    NERVOUS    SYSTEM. 

dation  in  nerve-trunk;  swelling  and  degeneration  of  individual 
fibres ;  ( I )  axis  cylinder  broken  and  disintegrated  in  fatty  mass ; 
(2)  medullary  substance  separated  into  segments  and  fatty 
globules,  and  mingled  with  granules  and  nucleated  cells;  (3) 
connective-tissue  sheath  shrunken  and  empty.  Nuclei  multiply. 
Products  of  degeneration  liquefy  and  are  absorbed. 


Fig.  "2. — Neuritis. 


Fig.  3. — Neuritis. 


Fig.  4. — Neuritis. 


Regeneration  occurs  by  growth  of  new  fibres  outward  from 
th.e  healthy  stump  into  the  old  sheath. 

2.  Interstitial  neuritis.  The  connective  tissue  of  the  endoneu- 
rium  and  perineurium  increases  in  volume  and  the  nerve-fibres 
are  compressed  by  the  congested  vessels  and  by  the  new  tissue. 
These  forms  usually  occur  together  in  non-traumatic  cases. 

Syiuptoins. — Weakness  or  paralysis  with  atrophy  and  reac- 
tion of  degeneration  in  muscles  supplied  by  nerves  involved.  Re- 
action of  degeneration  (R.  D.)  is  a  change  in  the  action  of  the 
nerves  and  muscles  to  the  electric  currents.  The  response  of  the 
nerve  to  both  currents  is  lost.  The  muscle  loses  its  faradic  reac- 
tion. The  galvanic  reaction  is  changed,  the  muscle  responding 
more  actively  to  the  closure  of  the  positive  pole  (anode)  than  to 
that  of  the  negative  pole  (kathode).  Pain  numbness  or  anzesthesia 
in  skin  supplied  by  nerve  involved.  Vasomotor  and  trophic 
changes  in  the  distribution   of  nerve   involved.      Coldness   from 


DISEASES    OF   THE    NERVOUS    SYSTEM.  9> 

sluggish  metabolism;  glossy  skin;  oedema;  pain  and  tenderness  at 
seat  of  inflammation  in  interstitial  cases,  and  along  the  nerve 
trunk. 

Course. — Slow  spontaneous  recovery  when  continuity  of 
nerve  is  preserved.    Otherwise,  no  recovery. 

Treatment. — If  nerve  is  broken  unite  divided  ends.  Rest  the 
part  injured  but  exercise  the  muscles  paralyzed  by  electricity  and 
massage.  Use  liot  applications,  sedative  lotions.  Protect  from 
cold  by  cotton  batting.     Morphine  for  pain. 


^Multiple  Neuritis. 

Multiple  neuritis  is  an  inflammatory  or  degenerative  disease 
of  the  peripheral  nervous  system  varying  in  extent  and  intensity 
and  affecting  symmetrical  parts  of  the  body. 

The  motor  nerves  may  be  involved  alone  {e.g.,  in  lead  and 
mercury  poisoning),  or  the  sensory  nerves  alone  (e.g.,  in  coal- 
gas  poisoning),,  or  both  may  be  involved  together  {e.g.,  in  al- 
coholic neuritis).  The  distal  parts  of  the  nerves  are  commonly 
affected  to  a  greater  extent  than  the  central  parts.  Hence  the 
symptoms  appear  chiefly  in  the  distal  parts  of  the  extremities. 

The  pathological  process  is  the  same  as  in  simple  neuritis 
and  may  be  parenchymatous  alone,  or  interstitial  alone,  or  both. 


Fig.  5— Neuritis  contracted  with  normal  nerve. 

Etiology.-^i.  Toxic  cases:  Alcohol,  lead,  arsenic,  bisulphide 
of  carbon,  copper,  mercury,  phosphorus,  coal  gas,  coal   tar   drugs. 


10  DISEASES    OF    THE    NERVOUS    SYSTEM. 

2.  Infectious  cases:  Diphtheria,  typhoid,  typhus,  scarlet  fever, 
-measles,  malaria,  leprosy,  small-pox,  erysipelas,  gonorrhea, 
grippe,  and  beri-beri. 

3.  Rheumatic  cases :  Exposure  to  cold,  overexertion. 

4.  Secondary  to  anemia,  gout,  tuberculosis,  syphilis,  sep- 
ticaemia, general  malnutrition,  and  diabetes. 

Syjiiplouis. — Acute  or  subacute  onset  with  fever,  103°- 
104°  F.,  and  general  febrile  symptoms — sometimes  without  fever, 

Sensory  Synipto)iis. — First  to  occur.  Pain — sharp,  severe, 
located  in  limbs,  increased  by  motion  or  pressure :  muscular  and 
nerve  tenderness,  sensitiveness. 

Parsesthesise — Burning,  tingling,  numbness,  band  about  legs 
and  body. 

Anaesthesia — In  tips  of  fingers  and  toes,  extends  up  limbs. 

Ataxia — In  fine  movements  and  loss  of  sense  of  position. 

Motor  Syiiipfoiiis. — Paralysis,  in  extensors,  dropped  wrist 
and  foot,  general  inability  to  walk  or  move  in  bed ;  contractures  ; 
cranial  nerves  may  be  paralyzed,  causing  symptoms  in  face  and 
eyes. 

Atrophy — Rapid  in  onset.  R.  D..  or  diminution  in  electric 
contractility ;  loss  of  deep  reflexes  ;  no  paralysis  of  sphincters. 

Trophic  Syuiptoms. — A'asomotor  paralysis ;  glossy  skin ; 
oedema ;  abnormal  growth  of  nails  and  hair :  sweating  profuse ; 
no  bedsores ;  urticaria. 

Certain  cases  present  peculiar  features  in  their  course. 

I.  AlcoJwIic  Xcurifis. —  {a)  Paralytic  type.  Rapid  onset  is 
the  rule,  with  delirium  and  delusions,  subsequently  imperfect 
memory  of  recent  events.  Severe  paralysis  in  extremities  with 
very  great  pain  :  anaesthesia  very  marked  in  hands  and  feet,  also 
tremor  and  tenderness;  dropped  wrists  and  feet;  or  (b)  Ataxic 
type.  Sharp  pains  are  soon  followed  by  great  ataxia  in  legs  and 
hands,  by  anresthesia  and  partial  paralysis  ;  but  no  loss  of  control 
of  bladder  or  rectum.  In  both  forms  there  is  danger  of  heart 
failure  or  death  from  exhaustion,  due  to  complicating  gastritis. 
Usually  there  is  rapid  increase  of  symptoms  for  three  or  four 
weeks,  and  then,  after  a  stationary  period  of  two  months,  a  slow 
progress  to  recoverv,  the  duration  b^'ing  from  six  to  twelve 
"months. 


DISEASES    OF     THE    NERVOUS    SYS'I'EM.  11- 

2.  Lead  Xcnritis. — Onset  with  intestinal  colic,  lead  line  on 
gums.  Paralysis  causing  dropped  wrists,  without  sensory  dis- 
turbance in  hands.  Deltoids  next  paralyzed.  May  affect  all 
muscles  of  arms  and  legs,  and  go  on  to  sensory  symptoms  with 
delusions,  but  this  is  rare. 

Gradual  recovery,  when  poison  is  eliminated,  in  four  months. 

3.  Arsenical  Cases. — Gastric  disturbance  at  outset.  Then 
paralysis  with  ataxia,  tremor,  atrophy,  and  great  numbness,  but 
little  pain  ;  legs  and  arms  equally  affected.  Skin  darkened.  Re- 
covery in  two  to  six  months,  depending  on  original  severity.  Con- 
tractures. 

4.  Coal-Gas  Cases. — Subacute  and  slight,  chiefly  sensory, 
numbness  for  a  long  time  in  fingers,  hands,  and  feet. 

5.  DipJifherific  Cases. — Severe  paralysis  of  all  extremities, 
usually  without  sensory  disturbance,  cranial  nerves  frec[uently 
affected.  It  begins  in  uvula,  and  swallowing  and  talking  become 
difficult.  Eyes  are  often  turned.  Ataxia  is  marked  in  some  cases. 
Never  pain.     Progress  to  recovery  usual  in  three  months. 

6.  Epidemic  Form.  (Beri-beri.)  Occurs  in  Brazil,  India, 
Borneo,  Japan,  PhiHppines.  Several  types :  acute  pernicious, 
chronic  oedematous,  chronic  atrophic.  Too  rare  to  need  attention 
here.     (See  Organic  Xervous  Diseases.     Starr.     Chap.  VIII.) 

Diagnosis  of  Multiple  Neuritis. — From  anterior  poliomyelitis  : 
by  pain,  tenderness  along  nerves,  sensory  symptoms,  distribution 
of  paralysis,  symmetrically.  From  locomotor  ataxia :  by  rapid 
onset  and  paralysis,  preservation  of  control  of  bladder,  and 
absence  of  Argyle-Robertson  pupil.  From  myelitis  :  by  absence 
of  affection  of  bladder  and  rectum,  by  absence  of  bedsores,  and 
lack  of  tenderness  of  spine  to  heat,  and  by  distribution  of  symp- 
toms in  periphery. 

Prognosis. — Good  in  large  majority  of  cases;  slow  recovery; 
bad  when  heart  becomes  rapid  and  respiration  poor. 

Treatment. — Rest  in  bed.  Warm  applications  to  limbs  by 
packs.  Rubbing  with  oil ;  gentle  massage  if  possible.  Prevent 
deformities  and  contractures  by  proper  position  of  limbs.  Elec- 
tricity, galvanism  through  nerves  and  to  muscles  after  acute 
stage.    Baths,  warm,  98°  F.,  for  half-hour  several  times  daily. 


n  DISEASES    OF   THE    NERVOUS    SYSTEM. 

Attention  to  diet,  nourish  well,  fatty  food,  cut  off  alcohol  in 
all  cases. 

General  and  nerve  tonics ;  iron,  quinine,  strychnine,  glycero- 
phosphate of  lime  and  soda 

In  acute  stage,  sodium  salicylate,  gr.  x.,  q.  3  hr.,  and  seda- 
tives, morphine,  phenacetine. 

In  chronic  stage,  arsenic  ^V  gr.  t.i.d.,  cod-liver  oil. 

Neuralgia. 

Neuralgia  is  a  painful  affection  of  the  sensory  neurone,, 
sometimes  functional,  sometimes  due  to  organic  changes  in  the 
sensory  ganglia. 

Causes. — Same  as  neuritis. 

Symptoms. — Spontaneous  pain  of  intense  character  in  the 
course  and  termination  of  a  single  nerve.  The  pain  occurs  in 
paroxysms,  is  not  continuous  like  neuritis.  Painful  points,  tender 
to  pressure  may  be  found,  but  the  entire  nerve  is  not  tender  as 
in  neuritis.     Herpes  Zoster  often  accompanies  neuralgia. 

Varieties  as  numerous  as  the  Jicrvcs.  Trigeminal,  Brachial 
Intercostal  Sciatic  most  common. 

Prognosis. — Good  except  in  organic  cases  and  in  trigeminal 
and  sciatic,  where  recurrence  is  the  rule. 

Treatment. — Remove  cause,,  if  found.  Locally  heat,  counter- 
irritation,  salicylates,  coal-tar  drugs,  opium,  gelsemium,  division 
of  nerves,  exsection  of  ganglia. 


DISEASES    OF    THE    XERVOUS    SYSTEM. 


13 


THE   SPIXAL   CORD  AND   CRAXIAL-XER\^E   NUCLEI. 


The  spinal  cord  in  man  is  made  up  of  thirty-one  segments — 
each  of  which  consists  of  a  mass  of  gray  matter  joined  to  a  pair  of 
spinal  nerves.  There  is  no  apparent  line  of  boundary  between  ad- 
jacent segments,  the  cord  being  a  long  cylindrical  organ.  But  in 
snakes  and  rabbits  the  area  of  gray  matter  is  much  larger  opposite 
the  entrance  of  nerves  than  between  them,  and  in  fishes  there  is  a 
visible  boundary  between  adjacent  segments. 

Each  segment  presents  a  symmetrical  arrangement  of  its  two 
halves.  Each  half  consists  of  a  central  mass  of  gray  matter 
surrounded  by  white  tracts.  Each  gray  mass  has  an  anterior  horn, 
a  central  mass,  and  a  posterior  horn.  To  each  horn  nerve-fibres 
are  joined,  making  the  anterior  and  posterior  nerve-roots.  The 
two  halves  are  separated  from  one  another  in  front  by  the  anterior 
fissure,  and  behind  by  the  posterior  septum.  They  are  joined  to- 
gether by  the  anterior  white  commissure  and  by  the  gray  commis- 
sure in  which  lies  the  central  canal  of  the  cord.  The  functions  of 
each  segment  are  shown  in  the  table  on  page  14. 


'.tlOO^* 


Fig,  6.— Cross  Section  of  Spinal  Cord.    (Gowers) 


14 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


2d      and      3d 
Cervical. 


4th    Cervical. 


5th    Cervical. 


6th   Cervical. 


rth    Cervical. 


Sth    Cervical. 


1st   Dorsal. 


2d    and    12th 
Dorsal. 


1st   Lumbar. 

2d    Lumbar. 

;id     Lumbar. 
4th     Lumbar. 

5th    Lumbar. 


Ist     and     2d 
Sacral. 


.3d    Sacral. 


4th    and    .jth 
Sacral. 


Sterno-mastoid.  Tra- 

pezius. 

Scaleni   and  neck. 

Diaphragm. 

Diaphragm. 

Deltoid. 

Biceps.  Coraco  -  bracli- 
ialis. 

Supinator    Lougus. 

Rhomboid. 

Supra-   &   infra-spinatus. 

Deltoid. 

Biceps    Coraco.-brachialis 

Brachialis   anticus. 

Supinator  longus. 

Supinator  brevis. 

Deep  muscles  of  shoul- 
der  blade. 

Rhomboid.    Teres   minor. 

Pectoralis    (clav.    part). 

Serratus    magnus. 

Brach.    anticus. 

Pectoralis    (clav.    part). 

Serratus  magnus. 

Triceps. 

Extensors  of  wrist  and 
fingers. 

Pronators. 


Triceps   (long  head). 

Extensors  of  wrist  and 
fingers. 

Pronators  of  wrist. 

Flexors    of    wrist. 

Subscapular. 

Pectoralis    (costal    part). 

Latissimus  dorsi. 

Teres  major.  ( 

Flexors  of  wrist  and 
fingers. 

Intrinsic  muscl«s  of 
liand. 

Extensors  of  thumb. 

Intrinsic    hand    muscles. 

Thenar  and  hypothenar 
eminences. 

Muscles  of  back  and  ab- 
domen. 

Ereetores  spinae. 


Ilio-psoas. 
Sartorius. 
Quadratus    lumb. 
Transversalis. 

Ilio-psoas.       Sartorius. 
Flexors  of  knee    (Remak) 
Quadriceps  femoris. 
Quadriceps  femoris. 
Inner    rotators   of    thigh. 
Adductors   of    thigh. 
Abductors    of    thigh. 
Adductors   of    thigh. 
Flexors  of   knee  (Ferrier) 
Tibialis  anticus. 
fJlutei. 

Biceps   femoris. 
Semi-tendinosis. 
f)utward    rotators. 
Flexors  of  ankle. 
Long  flexor  of  toes. 
Tibialis    post. 


I'croneus    longus. 
Intrinsic  muscles  of    foot 


Sjiliincter  ani  et  venicae 


Hypochondrium. 

Sudden  inspiration  pro- 
duced by  sudden  pressure 
beneath  the  lower  border 
of  ribs. 

Pupil   4-7   cervical. 

Dilatation  of  the  pupil 
produced  by  irritation 
of  neck. 


Scapular. 

Sth  Cervical  to  1st  Dorsal. 

Irritation  of  skin  over  the 
scapula  produces  con- 
traction of  the  scapular 
muscles. 

Supinator  Longus. 

Tapping  its  tendon  in 
wrist  produces  flexion  of 
forearm. 

Triceps. 

5th  to  6th  Cervical. 

Tapping  elbow  tendon  pro- 
duces extension  of  fore- 
arm. 

Posterior  wrist. 

6th  to  Sth  Cervical. 

Tapping  tendons  causes 
extension  of  hand. 


Anterior   wrist. 

7th  to  Sth  Cervical. 

Tapping  anterior  tendon 
causes  flexion  of  wrist. 

Palmar.     7thCerv.-lst  Dor. 

Stroking  palm  causes  clos- 
ure of  fingers. 


Epigastric.   4th-7th  Dorsal. 
Tickling    mammary    region 
causes  retraction  of  epi- 
gastrium. 
Abdominal.  7th-llth  Dorsal 
Stroking   side   of   abdomen 
causes  retraction  of  belly. 
Cremasteric.  lst-3d  Lumbar 
Stroking  inner  thigh  caus- 
es retraction  of  scrotum. 


Patella   tendon. 

Striking  tendon  causes  ex- 
tension of  leg.  2d-4th 
Lumbar. 


Gluteal. 

4tli-5th  Lumbar. 

Stroking  buttock  causes 
dimpling  in  fold  of  but- 
tock. 

Achilles   tendon. 

Over  -  extension  causes 
rapid  flexion  of  ankle, 
called    ankle   clonus. 

Babinski  reflex.  Scratch- 
ing sole  of  foot  causes 
retraction  of  great  toe. 

Plantar. 

Tickling  sole  of  foot  caus- 
es flexion  of  toes  and 
retraction    of    leg. 


Bladder  and   rectal  centre. 


Sensation. 


Back  of  head  to  vertex. 
Neck. 


Neck. 

Upper    shoulder. 

Outer  arm. 


Back     of     shoulder     and 

arm. 
Outer    side    of    arm    and 

foreaiTn. 
Anterior     upper     t  w  o- 
thirds   of   arm. 


Outer    side    of    arm    and 

forearm. 
Inside      and      front      of 

forearm. 


Inner    and   back    of    arm 
and    forearm. 


Radial      distribution     in. 
the    hand. 


Forearm  and  hand;    me- 
dian and  ulnar  areas. 


Ulnar  distribution  to- 
hand. 

Skin  of  chest  and  ab- 
domen, iu  bands  run- 
ning around  and  down- 
ward corresponding  to- 
spinal   nerves. 

Upper   gluteal   region. 

Skin  over  groin  and 
front  of  scrotum,  and 
narrow  band  down  the 
front  of  the  thigh  and 
leg. 

Inner  side  of  thigh. 

Outer  side  of  thigh. 


Inner  side   of   thigh   and 

leg  to  ankle. 
Inner  side   of   foot. 


Lower  gluteal  region 
back  of  thigh.  Leg 
and  foot  outer  part. 


Leg  and   foot  except   in- 
ner  side. 


Perineum    and    back    of 
scrotum.      Anus. 


DISEASES    OF   THE    NERVOUS    SYSTEM.  lo. 

The  Anterior  Horns  of  the  Spinal  Cord. 

These  vary  greatly  in  size  and  shape  in  various  segments,, 
being  large  opposite  the  entrance  of  the  cervical  and  lumbo-sacral 
nerves  and  thus  causing  the  cervical  and  lumbo-sacral  enlarge- 
ments of  the  cord. 

Their  size  and  shape  depend  upon  the  number  of  groups  of 
cells  found  at  different  levels  ;  for  the  horns  are  made  up  of  cells 
— large,  polygonal  cells  with  nucleus  and  nucleolus — collected 
into  distinct  groups. 

Some  groups  of  cells  lie  on  the  edge  of  the  horn,  making  pro- 
jections of  the  gray  mass  into  the  white  columns.  These  groups 
are  found  in  all  the  higher  vertebrates  and  are  not  peculiar  to 
man.  Other  groups  lie  within  the  horn  and  these  are  peculiar  to 
naan  and  the  higher  apes.  Each  group  of  cells  presides  over  the 
action  of  a  muscle  and  maintains  its  tone  and  nutrition,  so  that  all 
motor  impulses  to  the  muscle,  whether  reflex,  automatic,  or  vol- 
untary, proceed  from  the  group  of  cells.  The  outer  groups  gov- 
ern muscles  of  flexion,  extension,  pronation,  and  supination  of  the 
larger  joints.  The  inner  groups  govern  the  small  muscles  of  the 
fingers  and  toes.  Hence  the  outer  groups  are  said  to  preside  over 
fundamental  motions  and  the  inner  groups  over  accessory 
motions. 

The  thumbless  monkev  has  no  inner  groups  in  the  cervical 
region.  These  are  present  in  monkeys  with  thumbs  and  in  man. 
When  the  inner  groups  are  destroyed  by  disease,  the  finger  mo- 
tions are  paralyzed. 

In  each  segment  there  may  be  from  two  to  eight  groups  of 
cells.  Any  group  may  extend  through  several  segments.  If  a 
single  segment  is  destroyed  by  disease  several  muscles  will  be 
paralyzed.  But  no  muscle  will  be  totally  paralyzed  unless  its  en- 
tire group  of  cells  is  destroyed.  Total  paralysis  with  complete 
atrophy  in  a  muscle  indicates  destruction  of  the  entire  group  of 
cells  which  govern  the  muscle.  If  the  group  extends  through 
several  segments  the  paralysis  implies  disease  in  all  the  segments. 
The  table  shows  the  situation  in  the  various  segments  of  the 
group  of  cells  governing  the  various  muscles,  so  far  as  these  have- 
been  determined. 


16  DISEASES    OF    THE    NERVOUS    SYSTEM. 

Anterior  Poliomyelitis. 

Anterior  Poliomyelitis  is  a  disease  limited  to  the  anterior 
horns  of  the  spinal  cord.     It  may  be  acute  or  chronic. 

Acute  anterior  poliomyelitis  is  a  common  disease  of  childhood 
known  as  infantile  paralysis.  It  occasionally  occurs  in  adults. 
Chronic  anterior  poliomyelitis  is  an  uncommon  disease  of  adult 
life  or  old  age,  known  as  atrophic  paralysis. 

Acute  Anterior  Poliomyelitis.  Etiology. — Occurs  chiefly  be- 
tween 2  and  5  years,  when  exertion  is  greatest,  in  the  summer, 
June  to  September,  when  exposure  is  greatest  to  heat,  occasion- 
ally after  falls  and  after  fevers ;  it  is  probably  an  acute  infectious 
disease  in  two-thirds  of  the  cases.  In  the  other  third  it  is  prob- 
ably due  to  hemorrhage  from  or  to  thrombosis  in  a  spinal  blood- 
vessel. 

Pathology. — Lesion  is  an  acute  inflammation  of  the  entire 
gray  matter  of  the  anterior  horn,  the  cells  and  interlacing  fibres 
being  affected.  The  cells  become  swollen,  undergo  degeneration, 
and  liquefy,  and  then  shrivel  and  atrophy.  The  fibres  are  sepa- 
rated from  their  cells  and  atrophy.  The  neuroglia  is  infiltrated 
with  inflammatory  corpuscles.  The  capillaries  are  distended  and 
frequently  rupture.  The  process  may  go  on  to  complete  destruc- 
tion of  the  cells  or  may  be  arrested  at  any  stage. 

If  it  is  arrested  early,  repair  may  ensue  and  the  cells  regain 
their  former  appearance.  If  it  goes  on,  the  result  is  a  diminution 
in  the  size  of  the  horn,  a  change  in  its  shape,  and  a  contraction  of 
the  entire  cord  at  the  level  of  the  lesion. 

As  a  rule  the  entire  anterior  horn  is  at  first  involved,  but  the 
permanent  destruction  is  limited  to  one  or  two  groups  of  cells  on 
one  side  only. 

Inasmuch  as  each  motor  nerve-fibre  comes  from  and  is  a  part 
of  the  motor  cell,  the  nerve-fibres  degenerate  when  the  motor- 
cells  are  destroyed.  Atrophy  of  the  motor  nerve-roots  and  motor- 
nerves  from  the  anterior  horns  to  the  muscles  is  therefore  part  of 
the  lesion  in  anterior  poliomyelitis.  The  deformity  of  the  spinal 
cord  at  the  level  of  the  lesion  and  the  atrophy  of  the  nerve-trunks 
are  due  in  part  to  these  changes  in  the  nerve-fibres. 


DISEASES    OF    THE    NERVOUS    SYSTEM.  17 

The  muscles  which  are  paralyzed  atrophy  rapidly,  and  when 
recovery  does  not  occur  they  remain  small. 

While  no  special  groups  of  cells  are  known  to  control  the 
nutrition  of  the  bones,  it  is  found  that  if  the  gray  matter  near 
the  central  region  of  the  segment  is  destroyed  by  the  disease,  the 
bones  are  much  retarded  in  their  growth.  Hence  in  a  severe  case 
of  infantile  palsy  the  limb  affected  is  smaller  than  other  limbs  in 
all  its  parts.  But  trophic  changes  in  the  skin,  such  as  sores,  glossy 
skin,  or  gangrene,  do  not  occur.  Through  the  anterior  horns  pass 
fibres  from  the  central  region  which  control  the  vascular  tone  and 
metabolic  processes.  Hence  in  lesions  of  the  anterior  horn  symp- 
toms due  to  the  destruction  of  these  fibres  ensue,  viz.,  sluggish 
circulation,  cyanosis,  and  lowered  temperature,  with  imperfect 
nutrition. 

Sy)uptoms. — Sudden  onset  with  fever  lOo"  to  103°  F.,  occa- 
sionally without.  Febrile  symptoms :  Headache,  loss  of  appetite, 
nausea,  vomiting,  diarrhoea.  Restlessness  :  often  convulsions  and 
delirium.  The  fever  rarely  continues  more  than  two  to  three 
days.  Pain  in  the  back  and  limbs  is  complained  of  when  child  is 
old  enough  to  talk. 

Paralysis  appears  suddenly.  Sometimes  is  found  in  the 
morning :  is  complete  and  extensive  either  in  one  limb  or  more ; 
legs  oftener  than  arms,  4  to  i  ;  one  limb  more  than  the  other. 
^Maximum  is  reached  in  tirst  week.  Remains  stationary  for  two 
to  six  weeks  and  then  improves.  Result  is  recovery,  which  is 
partial ;  some  muscles  remain  paralyzed.  The  aff'ected  limb  atro- 
phies rapidly.  Atrophy  is  most  intense  in  the  muscle  permanently 
weak.  There  is  a  change  in  the  electric  reactions  in  the  paralyzed 
muscles.  R.  D.  Loss  of  faradic  excitement  in  two  weeks  or 
sooner.  Increase  at  first,  then  decrease,  in  galvanic  excitability. 
^Muscles  contract  slowly  instead  of  quickly,  more  forcibly  to  the 
positive  than  to  the  negative  pole. 

The  nutrition  of  the  entire  limb  suft'ers :  bones  small  and 
growth  impaired:  fat  is  less  firm,  and  skin  is  cold;  but  no  bed- 
sores appear.  The  sphincters  are  not  aff'ected.  The  reflex  action 
is  lost  at  the  level  aff'ected,  not  changed  elsewhere. 

Course. — There  is  a  progressive  improvement  which  begins 


18  DISEASES    OF   THE    NERVOUS    SYSTEM. 

within  two  months,  but  usually  some  muscles  remain  paralyzed 
and  atrophied,  and  the  joints  moved  by  these  may  become  de- 
formed ;  spine  curved.  The  muscles  most  frequently  affected  are : 
The  peronei  and  tibialis  anticus  in  the  leg — hence  talipes  equinus 
and  varus ;  the  muscles  of  the  calf  and  anterior  part  of  the  thigh ; 
the  deltoid,  biceps,  supinators,  and  spinati  in  the  arm — hence  sub- 
luxation of  humerus ;  the  muscles  of  the  hand  and  forearm. 

General  health  is  unaffected. 

In  adults  acute  anterior  poliomyelitis  presents  the  same 
symptoms,  but  fever  is  less  severe  and  pain  is  greater  in  muscles. 
Extent  of  initial  paralysis  is  greater.  Occasionally  the  onset  is 
slow,  so  that  case  is  called  subacute,  developing  in  two  to  four 
weeks  progressively,  remaining  for  a  time  stationary  and  then 
subsiding. 

Diagnosis. — From  acute  rheunaatism  in  infants.  Rheuma- 
tism may  produce  immobility  of  joints.  It  also  causes  pain,  red- 
ness, swelling  of  joints,  and  tenderness. 

Prognosis. — Good  as  to  life. 

As  to  recovery,  at  end  of  tzvo  weeks  test  faradic  reaction. 
The  muscles  in  which  it  persists  will  recover  entirely. 

At  end  of  three  months  test  again.  The  muscles  in  v/hich  it 
has  returned  will  recover  partially. 

At  end  of  six  months  test  again.  The  muscles  which  do  not 
respond  will  never  recover  entirely,  but  if  galvanic  reaction  is 
good  may  improve. 

As  to  use  of  limb,  it  depends  on  growth  of  bone ;  e.  g.,  short 
leg;  on  development  of  deformity  and  contractures;  e.g.,  talipes. 

Treatment. — In  acute  stage :  Cup  or  blister  the  spine  and 
keep  quiet.    Give  ergot  and  bromide,  and  antipyretics. 

In  chronic  stage :  Rubbing,  warm  clothing,  galvanism  to  the 
muscles,  interrupted,  continuous.  Strychnine  ^^  g-  to  •g'-g-  t.i.d.,  ac- 
cording to  age.  Prevent  or  remedy  deformities  by  apparatus  or 
surgical  operation. 

Chronic  Anterior  Poliomyelitis. — Progressive  muscular  atro- 
phy occurs  in  adults  between  thirty  and  fifty  years ;  is  a  rare 
disease. 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


19 


Etiology. — Falls  and  injuries,  exposure  to  damp  and  cold, 
alcoholic  and  sexual  excesses,  lead  poisoning   (?), 

Syuipfonis. — Gradually  increasing  atrophic  paralysis,  several 
months  in  onset,  preceded  by  fatigue  and  weakness  and  loss  of 
weight.     Aluscles  become  flabby,  then  atrophied  and  paralyzed. 

It  begins  in  legs  and  extends  upward  (peroneal  type). 

It  may  begin  in  hands  and  then  extend  to  shoulders  and  in- 
vade the  back  (Aran-Duchenne  type). 

Finally,  all  the  muscles  of  the  body,  including  face  and 
tongue,  may  be  affected.     The  tendon  reflexes  are  lost. 

There  are  fibrillary  twitchings  in  muscles. 

There  are  electrical  changes  which  vary  in  dififerent  cases ; 
usually  R.  D.  is  found. 

The  circulation  is  poor  in  the  limb,  skin  cold  and  blue. 

There  is  no  sensory  disturbance  except  slight  numbness. 

There  are  no  visceral  symptoms,  no  disturbance  of  bladder 
and  rectal  control.     Bedsores  do  not  develop. 

Course. — Gradual  increase  after  a  long  period  of  stationary 
state.    Sometimes  a  steady  progress  to  bulbar  paralysis  and  death. 

Treatment. — Similar  to  chronic  stage  of  acute  anterior  polio- 
myelitis. 

Cranial-Nerve  Nuclei. 

The  groups  of  cells  in  the  cerebral  axis  (medulla  oblongata, 
pons  Varolii,  and  crura  cerebri)  which  give  origin  to  the  motor 
cranial  nerves  lie  party  on  the  floor  of  the  fourth,  ventricle  (XII., 


Fig.    7. — Longitudinal    Section    Showing    the    Relative    Position    of    the    Cranial    Nerve 

Nuclei    (Edinger). 


20  DISEASES    OF   THE    NERVOUS    SYSTEM. 

VI.,  IV.,  III.),  and  partly  deep  beneath  the  floor  in  the  formatio 
reticularis  (XL,  IX.,  VII.,  Vm.).  These  groups  of  cells  are  quite 
homologous  to  the  groups  in  the  anterior  horns  of  the  cord,  and 
are  subject  to  diseases  whose  pathology  is  the  same  of  that  of 
poliomyelitis. 

Bulbar    Paralysis — or    Glosso-Labio-Laryngeal    Paralysis, 

(Rare). 

Symptoms. — Slowly  progressing  paralysis  with  atrophy  in 
the  muscles  supplied  by  the  motor  cranial  nerve  nuclei. 

1.  Disturbance  of  speech.  Alalia,  tongue  letters,  R  L  D  T, 
due  to  paralysis  of  XII.  nerve  nucleus.  Atrophy  and  tremor  of 
tongue  with  paralysis.     Chewing,  swallowing  impaired. 

2.  Muscles  of  lips  and  face  become  weak  and  thin,  due  to 
paralysis  of  VII.  nerve  nucleus.  Alalia  extends  to  lip  letters,  P  B 
V  F.  Atrophy  and  tremor  of  lips  with  paralysis.  Whistling, 
facial  expression  impaired.     Saliva  runs  and  is  increased. 

3.  Muscles  of  pharynx  and  larynx  affected,  due  to  paralysis 
of  the  IX.  and  XI.  nerve  nuclei.  Food  regurgitates  or  cannot  be 
swallowed ;  reflex  action  impaired ;  larynx  unprotected ;  voice 
monotonous,  low ;  cough  impossible. 

There  is  no  change  of  sensation  or  of  taste. 
Pulse  sometimes  rapid,  100  to  130. 
Duration,  two  to  five  years. 
Death  from  inanition,  pneumonia,  heart  failure. 

Ophthalmoplegia. 

This  is  a  rare  disease,  due  to  an  atrophy  of  the  nuclei  of  the 
nerves  moving  the  eyeball  or  to  hemorrhage  into  them. 

The  muscular  apparatus  of  the  eye  consists  of  external  mus- 
cles moving  the  eyeball :  Recti  and  obliqui  and  levator  palpebrse. 
Internal  muscles  moving  the  iris  :  Dilators  and  constrictors.  Each 
of  these  may  be  affected  alone  or  together. 

_    ,   ,    ,         1     .       (  externa. 
Ophthalmoplegia    ]  .^^^^^^ 

Ophthalmoplegia  Externa.     Symptoms. — Gradually  increas- 


DISEASES    OF    THE    NERVOUS    SYSTEM.  21 

ing  loss  of  "power  in  all  the  muscles  of  eyeball.  One  or  more 
muscles   at  first,  then  others,  till  all  are  affected. 

Result,  ptosis.  \'arious  forms  of  strabismus,  nystagmus,  and- 
finally  immobility  of  eyeball.     Double  vision. 

Ophthalmoplegia  Interna.  Symptoms. — Loss  of  reflex  to- 
light.  Occurs,  as  a  symptom  in  locomotor  ataxia  and  general 
paresis. 

Diag)iosis. — From  paralysis  of  single  nerves,  III.  nerve  or 
VI.  nerve,,  by  the  fact  that  such  disease  is  unilateral  and  all  the 
muscles  supplied  by  the  single  nerve  are  involved,  others  remain- 
ing unaffected,  and  by  the  fact  that  the  pupil  is  always  affected. 

Progressive  ^Muscular  Dystrophy. 

This  is  a  primary  muscular  disease  which  results  in  atrophy 
and  paralysis.  It  is  commonly  mistaken  for  chronic  anterior 
poliomyelitis  or  progressive  muscular  atrophy,  but  dift'ers  from 
this  in  causation,  symptoms,  and  pathology. 

Causation. — It  is  an  hereditary  aft'ection,  or  a  disease  of  de- 
velopment or  of  nutrition.  It  develops  in  several  children  in  same 
family  with  same  or  various  types. 

Pathology. — The  lesion  is  an  essential  and  primary  change 
in  the  muscle  fibres. 

1.  Individual  fibres  become  hypertrophied. 

The  nuclei  of  the  muscle  fibres  are  increased  in  number. 
The  vacuoles  appear  as  evidence  of  degeneration  and  fibres  split 
up.  At  the  same  time  there  is  an  increase  in  connective  tissue 
about  the  muscle  fibres.  Sometimes  there  is  a  development  of  fat 
between  the  muscle  fibres. 

2.  Subsequently  to  the  hypertrophy  and  sometimes  without 
it,  atrophv  of  the  muscle  fibres  occurs  with  same  development  of 
fat  and  connective  tissue  or  without  it. 

Appearance  during  hypertrophy  is  a  very  fat  limb  in  which 
muscles  are  really  w^eak ;  during  atrophy  is  a  very  thin  limb  in 
which  muscles  are  very  weak  or  even  totally  paralyzed. 

Symptoms. — In  all  forms  there  develops  a  progressive  sim- 
ultaneous weakness  and  atrophy  of  the  muscles  affected,  going 


22  DISEASES    OF    THE    NERVOUS    SYSTEM. 

on  slowly  to  complete  paralysis.  The  consequences  of  such  par- 
alysis are  evident  in  size,  posture,  and  deformities,  use,  motion, 
and  gait.  No  fibrillary  twitching  z's.  progressive  muscular  atro- 
phy. No  R.  D.  I's.  chronic  anterior  poliomyelitis.  No  sensory 
disturbance,  bladder,  or  rectal,  or  trophic  skin  changes. 

Various  types  of  the  disease  classified  by  Erb : 
I.  Infantile  muscular  dystrophy. 

1.  Hypertrophic  in  type. 

Pseudo-hA'pertrophy — fat  only. 
True  hypertrophy,  muscle  also. 

2.  Atrophic  type. 

In  limbs  only. 
In  limbs  and  face  also. 
II.  Adult  muscular  dystrophy,  with  similar  classes. 

I.  Infantile  Muscular  Dystrophy. — Hypertrophic  Form, 

1.  Pseudo-hypertrophic  Paralysis. — Children  aged  from  two 
to  eight  affected,  males  more  than  females.  Only  twenty-five  per 
cent,  occur  after  twenty  years.     Several  in  one  family. 

Begins  with  difficulty  in  gait.  Cannot  walk,  go  up-stairs,  or 
get  up.  Muscles  of  back  atrophied,  and  calves  of  legs  hypertro- 
phied.  Also  infraspinatus  and  deltoid  hypertrophied.  Other 
muscles  atrophy,  pectorales,  latissimus  dorsi,  triceps,  and  muscles 
of  thighs. 

Posture,  shoulders  far  back.  Gait  is  waddling,  and  mode  of 
rising  by  climbing  up  the  legs  due  to  paralysis  of  extensors  of  hip 
is  characteristic.  Finally,  inability  to  sit  up  from  paralysis  of 
trunk. 

After  paralysis  has  occurred  shortening  of  muscles  follows, 
and  deformities,  talipes  equinus,  and  curvature  of  spine  develop. 

No  R.  D.  Knee-jerk  normal,  then  weak.  Sensation  and 
sphincters  not  involved. 

Death  is  due  to  some  intercurrent  malady,  occurs  between 
twelve  and  twenty  years  of  age. 

Treatment. — Massage.     Thyroid  extract. 

2.  True  Hxperfrophic  Paralysis   (juvenile  muscular  dystro- 


DISEASES    OF    THE    NERVOUS    SYSTEM.  23 

phy).  Develops  in  children  six  to  ten.  Several  in  a  family.  Be- 
gins with  progressive  weakness  of  muscles. 

Muscles  affected  with  hypertrophy  are  deltoid,  infraspinatus, 
muscles  of  forearm,  sartorius,  gastrocnemii. 

Muscles  which  atrophy  are :  pectorales,  latissimus  dorsi,  ser- 
ratus  magnus,  biceps,  coracobrachialis,  supinator  longus,  adduc- 
tors of  thighs,  glutei  and  back  muscles  ;  finally,  calf  and  peronei. 

Gait,  posture,  and  deformities  are  characteristic.  No  fibril- 
lary contraction.  No  R.  D.  Knee-jerk  slowly  diminished.  No 
disturbance  of  sensation  or  of  sphincters. 

3.  Atropine  Type  in  Body  and  Limbs  (hereditary  muscular 
atrophy).  Same  features,  except  entire  absence  of  hypertrophy. 
Develops  from  eight  to  ten  years. 

4.  Atrophie  Type  in  Limbs  and  Faee  (infantile  muscular 
atrophy;  Landouzy-Dejerine  type).     Face  is  often  first  affected. 

When  face  is  involved  the  zygomatic  muscles  are  affected 
first ;  loss  of  naso-labial  fold ;  flat  mask-like  face ;  lower  lip  pro- 
jects;  orbicularis  is  affected;  lips  open;  labials  can't  be  spoken. 
Sometimes  orbic ;  palpebrse  weak.  Facial  muscles  atrophy  slowly. 
The  other  muscles  of  the  body  are  affected  in  succession  much 
later,  pectorals,  latissimus  dorsi,  biceps,  and  triceps.  Deltoids 
may  be  hypertrophied.  Back  muscles  and  extensors  of  thighs  are 
invaded. 

Gait,  posture,  same  as  in  other  types. 

Any  of  these  types  may  go  on  to  another  type. 

II.  Adult  Muscular  Dystrophy. 

Any  of  these  forms  may  occur  in  adults.  Usually  a  family 
history  can  be  obtained.  Usually  develops  about  age  of  eighteen, 
sometimes  not  till  thirty.  Some  muscles  are  hypertrophied,  others 
atrophied  as  in  infantile  types. 

The  Central  Gray  Matter  of  the  Spixal  Cord  and  its 

Diseases. 

The  portion  of  gray  matter  lying  behind  the  anterior  horn, 
and  adjacent  to  the  central  canal  of  the  spinal  cord  and  extending 


24  DISEASES    OF    THE    NERVOUS    SYSTEM. 

backward  to  the  posterior  horn,  is  made  up  of  gelatinous  gray 
substance  and  of  scattered  nerve-cells  with  a  plexus  of  fibres. 
It  contains  one  long  column  of  flask-shaped  cells — the  column  of 
Clarke — in  its  posterior  median  part ;  and  an  irregular  column  of 
small  cells  in  its  lateral  part — the  intermedio-lateral  column.  The 
majority  of  these  cells  differ  from  the  cells  of  the  anterior  horn, 
in  not  having  a  long  axis-cylinder  process  which  enters  a  nerve. 
They  have  numerous  branching  processes,  some  sending  a  long 
branch  to  the  other  side  through  the  anterior  commissure,  others 
sending  a  branch  out  into  the  antero-lateral  column  where  it  bifur- 
cates, turning  up  and  down,  and  in  its  course  gives  off  collaterals, 
which  enter  the  gray  matter  at  various  levels.  These  cells  thus 
form  an  associated  system  within  the  cord. 

The  function  of  the  central  gray  matter  is  to  preside  over,  i, 
vasomotor  tone ;  2,  nutrition  of  all  parts ;  3,  visceral  activity,,  in- 
cluding digestion  and  excretion,  and  the  activities  regulated  by 
the  sympathetic  system. 

1.  Vasomotor  innervation  is  a  reflex  matter  requiring  centres 
with  sensory  and  motor-nerves.  Gaskell  has  proven  that  these  lie 
in  the  central  gray  matter  and  are  joined  by  fine  nerve-fibres 
which  pass  in  the  nerve-roots  through  the  two  horns  of  the  cord. 
The  regulation  of  the  flow  of  blood  in  accordance  with  the  need 
of  an  organ  is  governed  here. 

2.  The  proper  degree  of  metabolism  necessary  for  nutrition 
in  the  skin,  bone,  and  joints  and  muscles,  or  for  repair  of  tissue, 
is  under  the  control  of  nerves  whose  centres  are  in  the  central 
gray  matter. 

3.  The  sympathetic  system  of  nerves  presides  directly  over 
digestion,  circulation,  secretion,  and  excretion,  but  is  in  turn  con- 
trolled by   spinal   centres  which  lie  in  the   entire  length  of  the 

•  spinal  cord  in  the  central  gray  matter. 

The  central  gray  matter  receives  sensory  impulses  of  pain 
and  temperature  sense,  and  transmits  these  for  some  distance  on 
their  way  upward  after  they  reach  it  through  the  posterior  nerve- 
roots  ;  each  segment-  of  the  cord  being  related  to  its  own  part  of 
the  surface,  as  shown  in  the  table. 

All  these  functions  are  disturbed  in  diseases  of  the  central 
gray  matter. 


DISEASES    OF   THE    NERVOUS    SYSTEM.  25 

Syringomyelitis. 

Pathology. — This  is  a  rare  disease,  usually  of  congenital 
origin,  characterized  by  a  development  of  gliomatous  tissue  in  the 
gray  matter  around  the  central  canal,  which  subsequently  ex- 
tends outward,  involving  the  entire  central  gray  matter,  and  then 
degenerates  and  is  absorbed,  leaving  a  cavity  in  the  spinal  cord. 
Such  a  cavity  may  extend  through  a  part  of  the  cord,  or  through 
its  entire  length  ;  varying  in  size  at  different  segments  and  thus 
destroying  more  or  less  of  the  gray  matter.  Its  usual  situation  is 
in  the  the  lower  cervical  and  upper  dorsal  regions.  The  disease 
may  invade  the  anterior  horns  of  the  cord,  causing  the  symptoms 
of  chronic  anterior  poliomyelitis.  It  may  invade  the  posterior 
horns  and  columns,  causing  symptoms  of  posterior  sclerosis. 
Sometimes  spinal  gliosis  develops  in  adult  life  and  goes  on  to 
the  formation  of  a  cavity.  Sometimes  long  perforating  hemor- 
rhages occur  in  the  cord,  and  when  the  clot  is  absorbed  a  cavity 
remains.  Sometimes  local  softening  in  the  cord  leads  to  the 
formation  of  a  cavity.  Any  disease  destroying  the  central  gray 
matter  of  the  cord  causes  the  symptoms  of  syringomyelitis. 

Symptoms. — i.  Loss  of  the  sensations  of  temperature  and 
pain  while  the  sensations  of  touch  and  location  are  retained.  The 
distribution  of  this  sensory  disturbance  depends  on  the  location 
of  the  disease,  e.  g.,  if  the  left  hand  and  forearm  only  are  thus 
affected,  the  disease  must  be  limited  to  the  left  side  of  the  cervical 
region  of  the  cord  in  its  lower  third,  which  receives  sensations, 
from  these  parts.  Such  disturbance  of  sensation  may  be  exten- 
sive, involving  irregular  areas  of  the  body.  It  is  never  symmet- 
rical on  both  sides. 

2.  Vasomotor  and  trophic  symptoms.  Cyanosis,  oedema, 
blueness  of  extremities,  with  lowering  of  temperature,  ulcers,  bul- 
lous eruptions,  sweating,  thickened  or  glossy  skin,  defective 
growth  of  the  nails,  great  brittleness  of  the  bones  leading  to  re- 
peated fractures,  and  joint  affections,  also  progressive  atrophy  of 
the  muscles.    These  occur  usually  in  one  limb  only. 

3.  Disturbance  in  and  loss  of  control  over  the  action  of  blad- 
der and  rectum,  and  loss  of  sexual  power,  are  present  when  the 
lumbar  region  of  the  spinal  cord  is  invaded. 


•36  DISEASES    OF   THE    NERVOUS    SYSTEM. 

4.  Paralysis  of  the  spinal  muscles  with  curvatures  of  the 
spine. 

Course  of  the  disease  is  chronic,  with  slow  progress  till  the 
symptoms  are  developed,  often  including  the  symptoms  of  chronic 
anterior  poliomyelitis.  It  then  remains  stationary,  but  if  it  ad- 
vances upward  and  invades  the  medulla,  death  may  occur  at  any 
time  from  paralysis  of  the  heart  and  respiration. 

The  prognosis  is  bad  and  no  treatment  can  stop  the  course. 

When  tumors  destroy  the  central  gray  matter  or  hemor- 
rhages occur  in  it,  the  same  terminal  symptoms  may  be  expected 
as  in  syringomyelitis. 


The  Posterior  Horns  of  the  Cord. 

This  portion  of  the  cord  is  made  up  partly  of  gelatinous  mat- 
ter which  occupies  its  extremity,  and  partly  of  a  fine  plexus  of 
nerve-fibres,  in  which  small  cells  are  irregularly  scattered.  The 
function  of  the  posterior  horn  is  to  receive  the  impulses  coming 
in  through-  the  posterior  nerve-roots,  and  to  transmit  such  im- 
pulses in  various  directions.  These  are  the  sensations  of  touch, 
temperature,  pain,  pressure,  and  location,  and  of  the  muscular 
sense. 

Each  nerve  of  sensation  gives  off  numerous  branches  on 
■entering  the  cord,  and  finally  terminates  in  a  brush-like  expansion 
of  nerve-fibrils  which  surrounds  some  nerve-cell,  or  in  the  plexus 
of  nerve-fibrils  which  make  up  a  fine  felt-like  tissue  in  the  pos- 
terior horn.  Any  fibre  after  entering  the  posterior  nerve-root 
may  pass  directly  into  the  posterior  horn,  or  may  turn  up  or  down 
in  the  white  matter  near  the  horn  at  some  level  other  than  that 
of  its  entrance.  The  posterior  horns  are  continuous  upward 
(through  the  medulla  and  pons)  with  the  ascending  root  of  the 
fifth  nerve.  The  diseases  of  the  posterior  horn  will  be  considered 
with  diseases  of  the  posterior  roots  and  columns,  as  they  uni- 
formly coincide. 


DISEASr':S    OF     THE    NERVOUS    SVS'fEM.  27 

The  White  Columns  of  the  Spinal  Cord  and  their 
Diseases. 

The  gra}-  matter  of  the  spinal  cord  is  surrounded  by  white 
tissue  made  up  of  anterior  and  posterior  nerve-roots  and  of  nerve- 
fibres  passing  up  or  down  the  cord  for  longer  or  shorter  distances. 
The  white  columns  contain  therefore : 

1.  Fibres  joining  the  skin,  joints,  muscles,  and  viscera  to  the 
gray  matter  of  the  spinal  cord  and  entering  the  various  segments 
through  the  anterior  and  posterior  nerve-roots. 

2.  Fibres  connecting  the  various  segments  with  one  another. 

3.  Fibres  joining  the  various  segments  with  the  brain. 

The  white  matter  can  be  divided  into  different  columns  by 
observing  the  process  of  development — different  columns  develop 
at  dift'erent  periods  of  foetal  life ;  or  by  studying  the  process  of 
disease — different  diseases  select  different  columns. 

These  columns  and  their  diseases  are  as  follow^s : 

The  Motor  Coluj/;ns. 

1.  Anterior  median  eoliiniii. 

2.  Lateral  pyramidal  column. 

.At  the  lower  limit  of  the  medulla  each  anterior  pyramid  di- 
vides into  two  parts ;  one  part  passes  directly  on  into  the  anterior 
median  column  of  the  cord :  the  other  part  crosses  over  to  the 
opposite  lateral  column  of  the  cord,  lying  near  to  the  grav  matter 
in  the  angle  between  the  anterior  and  posterior  horn.  As  the 
fibres  making  up  these  columns  pass  down  the  cord,  they  turn 
into  the  anterior  grav  horns  of  the  diff'erent  segments — each  col- 
umn becoming  smaller  the  low^er  it  goes.  The  anterior  median 
column  is  exhausted  at  the  lower  dorsal  cord,  and  therefore  does 
not  exist  in  the  lumbar  region.  The  lateral  pyramidal  column 
extends  to  the  lowest  segment  of  the  cord.  These  columns  trans- 
mit motor  impulses  from  the  motor  cortex  of  the  brain  and  from 
the  motor  ganglia  of  the  brain  to  the  spinal  motor  centres.  These 
columns  also  contain  fibres  whose  origin  is  in  the  pons  and  the 
cerebellum,  which  pass  with  the  motor  fibres  from  the  brain, 
and  terminate  in  the  anterior  horns  of  the  cord. 


28 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


They  also  contain  fibres  of  association 
passing-  between  various  segments  of 
the  cord.  All  these  sets  of  fibres  de- 
generate downward.  The  area  of  de- 
generation is  less  in  extent  when  the 
lesion  is  in  the  brain  than  when  it  is  in 
the  cord  itself. 

Lateral  Sclerosis. 

Lateral  sclerosis  is  a  chronic  sclerotic 
process  affecting  the  lateral  pyramidal 
colums  of  the  spinal  cord. 

It  may  be  primary  and  is  then  bi- 
lateral. 

It  may  be  secondary  to  other  dis- 
eases in  the  brain  or  cord  which  sepa- 
rate the  fibres  of  the  motor  tract  from 
their  centres  of  origin  and  nutrition  in 
the  brain  cortex.      Such  diseases  are: 

1.  Tumors,  softening  or  hemorrhage 
in  the  brain,  destroying  the  motor  tract 
in  one  hemisphere,  in  which  case  the 
secondary  sclerosis  is  found  in  the  ante- 
rior median  column  and  the  opposite 
pyramidal  tract. 

2.  Congenital  maldevelopment  of 
the  brain  and  hydrocephalus,  affecting 
both  motor  tracts,  in  which  case  both 
anterior  median  and  both  lateral  col- 
umns are  sclerotic. 

3.  Any  lesion  in  the  spinal  cord, 
either  unilateral  or  bilateral,  or  com- 
pression of  the  cord  by  disease  of  the 
vertebrae,   in  which   case    the    sclerosis 


Fig.  8. — The  Motor  Tracts.  Py,  lateral  pyramidal;  AM,  anterior  median  column,  both 
from  right  pyramid  of  medulla  to  motor  neurones  of  anterior  horn,  whence  motor 
nerves  (w)  pass  to  muscles;  s,  sensory  nerve  entering  posterior  horn  and  posterior 
root  zone  of  the  column  of  Burdach  (B),  and  sending  fibres  to  (a)  association- 
neurones;  (c)  comniissuralilcurones,  and  also  to  motor  neurones,  in  anterior  horn; 
h,  fibres  of  lateral  tract  consisting  of  association-fibres  between  various  segments. 


DISEASES    OF     IHE    NERVOUS    SYSTEM.  29 

-only   appears   below  the  level  of  the  lesion,   and  its  extent  is 
greater  in  area  than  in  1  or  2 

Pathology  of  Sclerosis. — i.  An  increase  in  the  thickness  of 
the  connective-tissue  framework  which  supports  the  nerve-fibres. 
2.  A  primary  degeneration  or  a  secondary  destruction  of  the  axis 
cylinder  in  each  nerve-fibre,  resulting  in  its  swelling,  segmenta- 
tion, fatty  degeneration,  and  final  absorption.  The  result  is  to 
reduce  the  number  of  fibres  in  any  column  of  the  cord,  or  even  to 
destroy  them  entirely,  the  place  of  the  fibres  being  filled  by  con- 
nective tissue. 

Symptoms  of  Primary  Lateral  Sclerosis,  or  Spastic  Paraple- 
gia.— A  weakness  and  stififness  in  motion,  beginning  in  the  legs 
and  ascending,  finally  involving  the  arms.  The  muscles  affected 
do  not  atrophy  rapidly,  as  their  spinal  centres  are  not  diseased. 
Their  reflex  and  mechanical  excitability  is  increased,  as  the  spinal 
centres  are  no  longer  inhibited  by  brain  impulses.  Hence  in- 
creased knee-jerk  and  ankle  clonus  are  present.  They  become 
rigid  from  the  increased  spinal  activity.  Hence  the  gait  is  at  first 
"spastic"  (toes  drag,  knees  overlap,,  motion  stiff)  ;  finally,  when 
paralysis  is  complete,  the  legs  are  drawn  up,  knees  overlapping 
and  so  rigid  as  to  be  incapable  of  passive  motion.  There  are  no 
electric  changes  in  the  muscles. 

The  action  of  the  bladder  is  imperfectly  controlled,  and 
finally  involuntary  emptying  of  the  bladder  at  intervals  or  reten- 
tion of  urine  occurs.  Constipation  is  obstinate.  In  some  cases 
of  primary  lateral  sclerosis  the  bladder  and  rectum  are  not  affect- 
ed. The  vascular  tone  is  decreased  toward  the  close  of  the  dis- 
ease and  nutrition  is  impaired.     There  are  no  sensory  symptoms. 

Course  of  the  Disease. — The  symptoms  develop  slowly  and 
increase  until,  after  many  years,  permanent  paralysis  has  de- 
veloped. 

Secondary  Lateral  Sclerosis  presents  the  same  symptoms  on 
one  or  both  sides,  but  the  symptoms  develop  more  rapidly  accord- 
ing to  the  nature  of  the  primary  disease. 

Diagnosis  between  lateral  sclerosis  and  anterior  poliomyelitis  : 

Lesion  in  pyramidal  tracts.  Lesion  in  anterior  gray  horns. 

Paralysis  usually  on  both  sides  Paralysis  may  be  limited  to  an\'  sin- 
equally,  in  legs,  or  in  legs  and  gle  limb,  and  rareh^  affects  both 
arms,  never  in  arms  alone.  limbs  equally. 


30  DISEASES    OF    THE    NERVOUS    SYSTEM. 

All    muscles    are    about    equally    af-  Certain  groups  of  muscles  only  are 

fected.     No   muscles   are    entirely  affected.     Others  escape  wholly. 

normal. 

Muscular  tone  is  heightened.  Muscular  tone  is  diminished. 

Tendency  to  rigidity  appears.  Muscles  are  relaxed. 

Reflex  excitability  is  increased.  Reflex  excitability  is  lost. 

Atrophy     is     absent,     or     is     slight;  Atrophy    is    always    present    in    the 

and   merely   due   to   disuse,    hence  paralyzed   muscles.      It   advances 

is    gradual    in    progress.      It    af-  rapidly,     and     may     become     ex- 

fects  the  entire  limb.  treme. 

Electric  contractility  is  unchanged.  Electric     contractility     is     changed. 

Reaction  of  degeneration  is  pres- 
ent within   two  weeks  of  the  on- 
set. 

Vascular  tone  is   diminished;   cyan-  J'ascular    tone    is     diminished,    but 

osis  and  oedema  may  occur.  oedema  does  not  occur. 

Paralyzed   limb    is   cold,    and    sweat  Paralyzed  limb  is  cool,  but  sweat  is 

may  be  increased.  not  increased. 

Trophic    disturbances    in    the    skin  Trophic  disturbances  in  the  skin  do 

are  not  infrequent.  not  occur. 

The    control    over   the    bladder    and  The    control    over    the   bladder    and 

rectum  may  be  diminished  or  lost.  rectum  is  not  impaired. 

Treatinciif. — None.     [Read  Strumpell  on  spastic  spinal  par- 
alysis and  on  compression  myelitis.] 


Amyotrophic  Lateral  Sclerosis. 

This  is  a  chronic  disease  affecting  the  entire  motor  system  of 
the  spinal  cord  and  cerebral  axis,  both  the  groups  of  cells  in  the 
anterior  horns  and  medulla  and  pons,  and  also  the  lateral  pyra- 
midal columns  in  the  cord  and  in  the  medulla  and  pons  being 
affected  together.  The  extent  of  the  sclerosis  is  greater  in  the 
cord  than  in  primary  lateral  sclerosis,  as  the  white  column 
which  lies  between  the  pyramidal  tract  and  the  gray  matter  (the 
lateral  limiting  column)  is  also  sclerotic  in  this  disease.  The 
changes  in  the  anterior  horns  are  the  same  as  in  chronic  anterior 
poliomyelitis. 

Symptoms. — The  symptoms  present  features  similar  to  those 
of  chronic  anterior  poliomyelitis  and  of  extensive  secondary  later- 
al sclerosis.  W'eakness,  paresis,  and  atrophy  begin  in  one  or  both 
arms  and  hands  and  increase  slowly.  The  muscles  of  the  hands 
and  the  extensors  of  the  wrists,  the  deltoid  and  triceps,  are  the 
muscles  chiefly  affected.  The  electric  contractility  is  diminished, 
and  finally  reaction  of  degeneration  appears.     The  muscular  irri- 


DISEASES    OE    THE    NERVOUS    SYSTEM.  31 

lability  and  reflexes  are  much  increased.  Finally  contractures 
result. 

Gradual  onset  of  spastic  paraplegia  in  the  legs  occurs  a  few 
months  after  the  arms  are  affected.  Spastic  gait  develops  with 
increased  reflexes.  In  the  final  stage  the  legs  are  totally  para- 
lyzed. There  are  no  sensory  disturbances,  and  bladder  and  rectum- 
are  usually  under  good  control. 

After  several  years  symptoms  of  bulbar  paralysis  gradually 
develop,  with  paresis  and  atrophy  of  face,  tongue,  and  throat, 
and  death  occurs  from  respiratory  paralysis.  Occasionally  the 
bulbar  symptoms  appear  early. 

The  course  is  a  slow  one.  The  disease  may  be  arrested,  but 
recovery  is  impossible. 

Diagnosis  from  myelitis  of  the  cervical  region  and  from 
syringomyelitis  by  the  absence  of  sensory  symptoms  ;  from  ante- 
rior poliomyelitis  chronica  by  increased  mechanical  and  reflex 
excitability  in  muscles  atrophied,  and  by  development  of  spastic 
gait. 

Treatment. — None. 

The  Sensory  Columns. 

3.  Posterior  Lateral  Column,  or  Column  of  Burdach. 

4.  Posterior  Median  Column,  or  Column  of  Goll. 

5.  Marginal  Column,  or  Column  of  Lissauer. 

These  columns  are  made  up  chiefly  of  sensory  fibres  which 
enter  the  cord  in  the  posterior  nerve-roots.  They  also  contain 
fibres  of  association  between  different  segments  of  the  cord.  Their 
subdivision  will  be  better  understood  b}^  a  study  of  the  course  of 
the  posterior  nerve-roots. 

The  posterior  nerve-roots  contain  fibres  which  arise  from  the 
cells  of  the  posterior  spinal  ganglia.  Each  spinal  ganglion  cell 
has  two  branches,  or  two  divisions  of  one  branch ;  one  going  out 
to  the  surface,  the  sensory  nerve ;  the  other  going  in  to  the  cord, 
the  posterior  nerve-root.  The  cell  in  the  ganglion  nourishes  both 
branches,  and  if  either  branch  is  separated  from  its  cell  it  degen- 
erates in  its  entire  length.  The  sensory  cranial  nerves  (X.,  IX.,. 
V.)  arise  from  similar  gangHa  (jugulare,  Gasserian). 

The  posterior  nerve-root  enters  the  cord  opposite  to  the  apex 


32 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


of  the  posterior  horn  and  then  divides  into  two  bundles,  a  median 
bundle  and  a  lateral  bundle. 

(1)  The  median  bundle  containing 
large  fibres  enters  the  column  of  Bur- 
dach,  forming-  its  root-zone  or  lateral 
zone.  Here  a  few  fibres  turn  down- 
ward into  the  segment  next  below 
(forming  the  comma-shaped  bundle  of 
Schultze)  and  end  in  the  posterior  horn; 
but  the  large  majority  of  fibres  turn 
upward  to  go  to  higher  segments. 
Some  of  these  soon  enter  the  inner  side 
of  the  posterior  horn  (short  fibres). 
These  lie  near  the  horn  in  the  lateral 
zone.  Others  pass  up  through  several 
segments  (medium  fibres).  These  lie 
nearer  to  the  median  line  and  in  the 
upper  cord  are  adjacent  to  the  column 
of  Goll,  forming  the  middle  .zone  of  the 
column  of  Burdach.  The  remainder 
pass  all  the  way  up  to  the  medulla  (long 
fibres),  lying  at  first  in  the  hinder  zone 
of  the  column  of  Burdach  and  later 
forming  the  column  of  Goll.  For  as 
each  root,  from  below  iipward,  enters 
the  cord,  it  displaces  inward  and  back- 
ward the  fibres  already  ascending;  so 
that  the  higher  the  level  the  larger  the 
number  of  ascending  fibres.  In  a 
cross-section  of  the  cord  in  the  upper 
cervical  region  the  long  fibres  which 
have  come  from  thelumbo-sacral  region 
occupy  the  column  of  Goll,  the  sacral 
fibres  lying  behind  the  lumbar;  the  long 
fibres  from  the  dorsal  region  occupy  the 
hinder  zone  of  the  column  of   Burdach ; 

Fig.  9. — The  Columns  of  Burdach  and  Goll  are  shown  on  the  left  side  of  the  cord.  The 
association-fibres  of  the  cord  joining  the  various  segments  with  each  other  of  various 
lengths  are  shown  passing  through  all  the  columns.  The  oval  column  of  Flechsig  is 
shown  in  the  lumbar  and  sacral  regions,  also  called  the  descending  septo-marginal 
tract. 


DISEASES    OE    'JHE    NERVOUS    SYSTEM.  iVd 

the  long-  fibres  from  the  cervical  region  occupy  the  middle  zone 
of  the  column  of  Burdach.  It  is  evident  that  there  is  no  phvsio- 
Jogical  distinction  between  the  columns  of  Goll  and  Burdach.  In 
the  anterior  part  of  both  columns  near  the  g'ray  commissure  lie 
association  fibres  and  commissural  fibres.  It  is  thus  evident  that 
the  median  bundle  of  posterior  nerve-root  fibres  constitutes  the 
columns  of  Burdach  and  of  Goll. 

The  final  termination  of  these  fibres  is  as  follows :  Each  fibre 
on  entering  the  cord  bifurcates,  a  short  branch  turns  down,  a 
long  branch  turns  up.  The  long  branch  in  its  course  upward 
gives  oil  collateral  branches  which  pass  into  the  gray  matter  of 
the  posterior  horn,  and  finally  the  branch  itself  ends  there.  In  all 
cases  the  termination  is  by  means  of  a  brush-like  expansion  of 
nerve-fibrils.  The  short  fibres  end  in  the  fine  network  making 
up  the  substantia  gelatinosa  of  Rolando  in  the  posterior  horn,  and 
about  the  cells  of  the  posterior  and  central  gray  matter.  The 
jnedium  fibres  end  in  a  network  which  surrounds  the  cells  of  the 
column  of  Clarke  in  the  central  gray  matter.  A  few  fibres  pass 
forward  to  the  anterior  horn  and  to  the  opposite  side  through  the 
posterior  gray  commissure.  The  long  fibres  pass  up  to  the  nuclei 
gracilis  and  cuneatus  in  the  medulla. 

(2)  The  lateral  bundle  of  the  posterior  nerve-root  consists  of 
both  large  and  small  nerve-fibres.  Many  of  these  pass  directly 
into  the  gray  matter  of  the  posterior  horn,  where  some  end  in  a 
network  of  fibres  about  the  cells  of  the  gelatinous  substance,  or 
■deeper  in  the  horn;  and  others  pass  forward  and  cross  over  in 
the  gray  commissure  to  the  opposite  side,  where  they  turn  out- 
ward into  the  antero-lateral  column  or  backward  into  the  column 
of  Goll.  The  smaller  fibres  bifurcate  on  entering  the  cord  and 
turn  down  and  up,  forming  the  column  of  Lissauer,  in  which 
they  pass  but  a  short  distance  and  then  turn  into  the  horn.  This 
column  is  of  uniform  size  through  the  cord,  and  hence  cannot  con- 
tain any  long  fibres. 

6.  Aiitcro-latcral  Ascending  Tract  or  Coliiiiin  of  Gon'crs. — 
In  the  antero-lateral  column  of  the  cord  lying  on  the  periphery 
just  in  front  of  the  direct  cerebellar  column  is  a  small  tract  which 
ascends  through  the  cord  and  enters  the  formatio  reticularis  of 


B4 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


the  medulla,  where  it  appears  to  end  in 
the  gray  cells  of  this  formation.  It  be- 
gins in  the  lumbar  region,  and  increases 
in  size  as  it  ascends,  receiving  fibres 
from  the  cells  of  the  central  gray  mat- 
ter. It  degenerates  upward.  It  has 
been  supposed  to  convey  sensations  of 
temperature  and  pain  upward  after  they 
have  passed  through  the  central  gray 
matter. 

7.  Direct  Cci'ebcllar  Cohnnn. — This 
column  lies  on  the  lateral  periphery  of 
the  cord  just  outside  of  the  pyramidal 
tract  and  behind  the  antero-lateral  as- 
cending tract.  It  is  very  small  in  the 
upper  lumbar  region,  becomes  larger  in 
the  dorsal  region,  and  is  of  consider- 
able size  in  the  cervical  region.  Its 
fibres  come  from  the  cells  of  the  col- 
umns of  Clarke  in  the  central  gray 
matter.  It  passes  into  the  restiform 
body  in  the  medulla  and  through  this 
into  the  cerebellum,  where  it  ends  in 
the  vermiform  or  middle  lobe.  It  is 
supposed  to  convey  sensations  of  equi- 
librium in  the  act  of  walking. 

It  is  evident  that  the  sensory  fibres 
from  the  posterior  nerve-roots  are  dis- 
tributed to  many  different  columns  of 
the  spinal  cord,  and  even  in  the  medulla 
have  numerous  different  connections. 
This  anatomical  fact  may  be  associated 
with  the  physiological  fact  that  one 
sensation  is  capable  of  producing  sev- 
eral different  effects,  c.g.^  a  burn  causes 
a  reflex  withdrawal  of  the  part  burned, 

Fig.  10. — On  the  right  side  the  termination  of  Sensory  Nerves  about  the  Cells  of 
Clarke's  Column  (C)  and  about  the  Intrinsic  Cells  (e)  is  shown.  From  C  fibres  pass 
up  in  D  C.the  direct  cerebellar  column.  From  e  fibres  pass  over  to  the  column  of 
Cowers  (G).  On  the  left  side  the  termination  of  sensory  fibres  about  intrinsic  cells 
(x)  is  shown.      From  x  fibres  cross  to  the  antero-lateral  column  and  ascend. 


DISEASES    OF    THE    NERVOUS    SYSTEM.  35 

vascular  changes,  and  a  process  of  repair,  sensations  of  heat, 
touch,  and  pain,  accurately  localized,  followed  by  conscious  effort 
to  protect  the  part :  e.  g.,  stumbling  in  the  act  of  walking  causes 
reflex  balancing  movements  involving  motions  of  the  entire  trunk 
and  arms  to  reestablish  the  centre  of  gravity  or  protect  against 
fall,  also  conscious  sensation  of  unstable  position,  possibly  vertigo, 
quickened  respiration,  action  of  ocular  muscles  and  head  to  ob- 
serve danger,  sensation  of  contact,  possibly  pain,  in  the  toes,  and 
corresponding  vascular  changes  locally,  and  finally  voluntary  ef- 
fort to  correct  position  after  an  appreciation  of  all  the  various 
sensations  received. 

We  distinguish  conscious  sensations  of  contact,  temperature, 
pain,  muscular  sense,  including  pressure  and  position,  and  uncon- 
scious sensations,  which  set  up  reflex  and  automatic  acts,  vascular 
changes,  variation  in  thermic  and  nutritive  processes,  and  changes 
in  muscular  tone.  These  all  enter  by  the  posterior  nerve-roots, 
and  set  up  activities  in  the  central  nervous  system. 

Locomotor  Ataxia. 

This  is  a  chronic  disease  of  the  sensory  part  of  the  nervous 
system,  the  posterior  nerve-roots  and  the  posterior  columns  of  the 
cord  being  diseased.  It  is  also  called  tabes  dorsalis,  or  posterior 
spinal  sclerosis. 

Pathology. — There  is  a  degenerative  neuritis  of  the  posterior 
nerve-roots,  and  sometimes  of  the  sensory  part  of  the  peripheral 
nerves.  There  is  a  sclerosis  of  the  posterior  columns  of  the  spinal 
cord,  beginning  in  the  lateral  or  root-zone  of  the  column  of  Bur- 
dach  and  in  the  column  of  Lissauer,  extending  thence  to  the  mid- 
dle zone  of  the  column  of  Burdach,  then  to  the  column  of  Goll, 
and  finally  to  the  hinder  zone  of  the  column  of  Burdach.  Thus 
both  posterior  columns  are  eventually  diseased  in  their  entire 
extent.  The  disease  usually  begins  in  the  lumbo-sacral  region  and 
extends  upward  through  the  cord.  It  is  many  years  before  it 
invades  the  cervical  region  or  destroys  the  entire  area  of  the  pos- 
terior columns.  The  terminal  network  of  nerve-fibres  in  the  pos- 
terior gray  matter,  and  especially  about  the  column  of  Clarke,  is 
destroyed  by  the  disease. 


36  DISEASES    OF    THE    NERVOUS    SYSTEM. 

Theories  of  the  disease :  ( i )  It  is  a  primary  sclerosis  of  the 
posterior  columns  of  the  cord.  (2)  It  is  a  sclerosis  of  the  root- 
zone,  due  to  disease  of  the  vessels  entering  this  zone.  (3)  It  is  a 
primary  disease  of  the  cells  of  the  posterior  spinal  ganglia,  with 
secondary  degeneration  of  the  sensory  fibres  entering  the  cord 
from  the  ganglia,  and  compensatory  sclerosis  in  their  course. 

Etiology. — It  is  a  disease  of  adult  life,  persons  under  twenty- 
five  rarely  being  aftected,  and  it  is  rare  among  women.  The  chief 
predisposing  cause  is  syphilis,  which  precedes  it  in  seventy  per 
cent,  of  the  cases.  The  exciting  causes  are  great  physical  exer- 
tion, exposure  to  cold  and  wet,  and  alcoholic  and  sexual  excesses. 

Symptoms. — The  symptoms  of  the  disease  are  very  numer- 
ous, but  appear  in  succession.  They  may  be  classified  according 
to  the  time  of  their  appearance.  There  is  a  stage  of  pain,  a  stage 
of  ataxia,  and  a  stage  of  paralysis. 

Symptoms  in  Stage  of  Pain. 

Paraesthesise.  Numbness,  formication,  sensation  of  dead  ex- 
tremities, cotton  or  pins  in  soles  of  feet  and  fingers,  coldness, 
itching  of  anus  and  scrotum  or  of  other  parts. 

Pain.  Short,  sharp,  cutting,  boring.  Deep  pain ;  comes  in 
attacks,  one  second  to  one-half  minute  repeated,  or  in  severe  at- 
tacks for  several  hours  or  days  with  intermissions,  rarel}-  con- 
tinuous attacks.  Begins  in  thighs  and  legs.  Pain  is  a  prominent 
symptom  early,  but  may  continue  through  all  stages.  It  may  be 
mistaken  for  rheumatism  or  sciatica,  but  its  character  is  different. 
It  is  the  same  as  in  alcoholic  multiple  neuritis,  but  there  tender- 
ness exists.  There  is  no  relation  between  intensity  of  pain  and 
degree  of  ataxia.  As  disease  advances  upward  the  pains  extend. 
Pain  may  be  absent  or  insignificant  in  some  cases,  especially  in 
cases  beginning  with  optic-nerve  atrophy. 

Pain  in  the  small  of  the  back  and  loins  of  an  aching  character 
may  occur. 

Girdle  sensation  or  sensation  of  tightness  and  pressure  in- 
tense and  severe,  about  the  legs  and  body.  This  ascends  grad- 
ually as  the  disease  advances. 

Loss  of  knee-jerk,  called  \\'estphars  symptom. 

Imperfect  control  of  bladder.     Slow  urination.     Slight  drib- 


DISEASES    OF    THE    NERVOUS    SYSTEM.  37 

bling,  and  hasty  urination.  I'^inally  control  is  very  imperfect  and 
may  be  painful.  This  may  be  a  dangerous  complication,  since 
death  from  cystitis  occurs. 

Impotence ;  occasionally  priapism  and  sexual  excitement  pre- 
cede this. 

Constipation  ;  usually  obstinate  throughout. 

Loss  of  pupil  reflex  to  ligbt,  the  reaction  in  accommodation 
being  preserved — Argyle-Robertson  pupil. 

Contracted  pupil,  "myosis  spinalis,"  is  frequent  but  not 
constant. 

Syiiiptoiiis  in  Stage  of  Ataxia. 

In  addition  to  those  of  first  stage  there  develop : 

An?esthesia  and  analgesia.  Sense  of  pain  impaired  and  de- 
layed. This  may  be  tested  with  faradic  brush.  It  prevents  in- 
juries from  being  perceived;  hence  ulcer  of  foot  and  Charcot 
joints  occur  as  complications.  Hence,  guard  against  accidents  in 
giving  hot  baths,  blisters,  etc. 

Hyperalgesia.  Sensation  of  pain  may  be  produced  by  any 
touch,  and  pain  is  felt  severely.  This  occurs  in  a  few  cases  early 
in  the  disease. 

Change  in  temperature  sensation.  Cold  felt  keenly  and  heat 
less  than  normal. 

Complete  anaesthesia  develops  late  in  the  disease  and  in  the 
extremities. 

Hypotonia  ;  an  undue  mobility  of  joints  from  lack  of  tone  in 
muscles. 

Impairment  of  muscular  sense.  Muscular  sense  is  the  sense 
by  which  the  situation  and  movements  of  the  limbs  are  appre- 
ciated, and  pressure  and  weight  are  felt.  Not  same  as  effort  sense. 
Imperfect  perception  of  weight  and  pressure  is  a  symptom  ob- 
served late.  Situation  of  limbs  is  imperfectly -perceived.  Hence, 
one  means  of  perfect  guidance  of  limbs  is  removed.  Hence,  pa- 
tient walks  badly  in  the  dark,  and  cannot  touch  objects  accurately 
with  eyes  closed  ;  hence  he  watches  his  own  motions — aiding  his 
muscular  sense  by  sight.  Therefore  a  blind  ataxia  is  the  most 
helpless  of  all. 

Ataxia  is  imperfect  co-ordination   of  muscular  action.     For 


38  DISEASES    OF   THE    NERVOUS    SYSTEM. 

every  compound  act  a  regular  succession  and  proper  degree  of 
motions  are  needed,  e.g.,  closure  of  fist,  walking.  This  regula- 
tion is  largely  automatic  and  is  carried  on  in  subcortical  centres, 
which  receive  unconscious  sensations  through  the  posterior  nerve- 
roots.  It  may  be  voluntary,  by  an  effort  of  attention,  and  is  so  at 
first,  for  all  motion,  and  always  for  highly  complex  motion,  e.g., 
writing.  Hence  ataxia  of  movement  may  occur  in  many  diseases. 
It  is  a  prominent  symptom  in  locomotor  ataxia. 

Romberg's  symptom — swaying  when  standing  with  eyes 
closed. 

Ataxic  gait — legs  wide  apart,  feet  lifted  too  high,  and  planted 
too  forcibly,  steps  being  of  irregular  length  and  body  imperfectly 
balanced. 

Imperfect  use  of  hands  in  dressing,  writing,  etc.  Irregular 
contraction  of  muscles  on  effort.    Imperfect  muscular  tone. 

Tests  of  ataxia.  Stand  with  eyes  closed,,  walk,  turn  suddenly 
or  walk  backward ;  touch  heel  to  toe,  or  heel  to  knee ;  touch  finger 
to  nose  or  both  fingers  with  eyes  closed ;  pick  up  pin ;  button 
clothes. 

Syniptonis  occasionally  present,  due  to  complication  of  neu- 
ritis in  various  nerves.  Optic-nerve  atrophy,  with  progressive 
blindness,  develops  in  ten  per  cent,  of  the  cases.  Optic  disc  looks 
white,  then  gray.  Arteries  appear  small  and  walls  thin.  Visual 
field  is  contracted  for  colors  and  for  light.  Finally  total  blindness 
occurs. 

Paralysis  of  the  ocular  muscles. 

VI.  n.  paralysis ;  convergent  strabismus,  with  contracted 
pupil. 

III.  n.  paralysis;  divergent  strabismus,  with  dilated  pupil  and 
ptosis.     Nystagmus  rarely  occurs. 

Deafness  develops  in  a  few  cases  from  atrophy  of  auditory 
nerve. 

Crises — (i)  gastric;  sudden  vomiting  with  pain,  for  several 
hours,  even  for  days.  Great  prostration  follows.  Rectal  feeding 
necessary.  Intestinal  and  rectal  crises  with  diarrhcea  and  tenesmus 
have  been  ol)served.  (2)  Laryngeal;  sudden  and  severe  cough, 
with  spasm  of  larynx  and  suffocation.      (3)   Cardiac;  attacks  of 


DISEASES    OF    THE    NERVOUS    SVS'IEM.  39 

angina  pectoris.  All  clue  to  a  complicating  peripheral  neuritis  in 
pneumo-gastric  nerve.     These  symptoms  are  quite  exceptional. 

Trophic  disturbances  are  more  common  in  stage  of  ataxia. 

Charcot  joints.  Knee,  elbow,  ankle,  wrist.  Enormous  swell- 
ing with  effusion  without  pain.  Erosion  of  ends  of  bones  and 
destruction  of  articulation.     Due  to  injury. 

Perforating  ulcer  of  foot,  caused  by  a  corn,  or  a  subcutaneous 
hemorrhage,  or  a  caries  of  bone  neglected. 

Rarefication  of  the  bones  with  production  of  fractures. 

Irregular  muscular  atrophies  develop  late  in  the  disease. 

Herpetic  eruptions  and  pemphigus. 

These  are  due  to  a  combination  of  causes,  chiefly  to  a  loss  of 
pain  sense  which  prevents  injuries  from  being  perceived,  or  to  a 
complicating  peripheral  neuritis. 

Syinpfoins  in  Stage  of  Paralysis. 

General  nutrition  remains  good,  but  ataxia  becomes  so  ex- 
treme as  to  render  patient  helpless  and  confine  him  to  bed. 

Control  of  bladder  completely  lost,  and  urine  dribbles  con- 
stantly. 

Accidents  produce  injuries,  and  trophic  disturbances  follow. 

Hence  patients  die  of  bedsores,  cystitis,  exhaustion,  or  of 
complicating  penumonia. 

Course  of  the  disease  is  chronic  through'  the  three  stages, 
lasting  twenty  to  forty  years. 

Usual  mode  of  onset  is  with  pain,  loss  of  knee-jerk,  bladder 
trouble,  impotence,  and  ataxia. 

Occasional  modes  of  onset:  (i)  blindness,  loss  of  knee-jerk, 
imperfect  gait,  numbness,  but  no  pain. 

(2)  Gastric  crises  at  intervals,  loss  of  knee-jerk,  then  pain 
and  ataxia. 

(3)  \'arious  forms  of  strabismus,  myosis.  then  ataxia  of 
arms. 

There  are  remissions  in  the  symptoms  and  complications  may 
subside,  but  no  true  arrest  occurs  or  recovery,  after  the  stage  of 
ataxia  has  begun. 

Diagnosis.  Early,  by  means  of  pains,  fatigue,  loss  of  knee- 
jerk,  and  Argyle-Robertson  pupil.  Late,  by  ataxia  and  bladder 
disturbance. 


40  DISEASES    OF    THE    NERVOUS    SYSTEM. 

Diagnosis  from  multiple  neuritis.     See  page  11. 

Treatment.  Moderate  exercise,  avoiding  all  fatigue.  Good 
general  diet  without  special  restrictions,  which  weaken  patient. 
Spinal  douches,  tepid  or  cool,  never  extreme.  Massage.  Practise 
in  fine  movements  to  overcome  ataxia.  Medicines — arsenic,, 
nitrate  of  silver,  ergot.     Anti-syphilitic  remedies. 

Treatment  of  pain  by  antipyrine,  etc.,  gelsemium,  opium,, 
faradization,  hot  applications.  Of  crises  by  counter-irritation  and 
morphine.  Of  optic  atrophy  by  strychnine.  Of  trophic  disturb- 
ances by  rest  and  apparatus. 

Combined  Sclerosis. 

This  is  a  Sclerosis  of  the  Lateral  and  Posterior  Columns. 
(rare). 

(i)  Congenital  cases.  Friedreich's  Hereditary  Ataxia  is  due 
to  defective  development  of  the  lateral  and  posterior  columns.  It 
occurs  in  several  members  of  a  family,  and  is  hereditary. 

Symptoms. — As  the  children  grow  up  they  are  found  to  be 
awkward.  They  walk  badly,  and  do  not  use  arms  well.  Reflexes 
are  lost,  exceptionally  exaggerated.  Dull  pains  in  legs,  not  light- 
ning in  character.  Deformity  in  feet.  No  bladder  symptoms, 
and  no  trophic  changes,  and  no  crises.  Ataxia  is  marked  and  goes 
on  to  actual  paralysis.  Speech  may  be  thick  and  nystagmus  pres- 
ent. The  condition  is  a  chronic  one,  lasting  during  life.  Chil- 
dren often  become  imbecile. 

(2)  Acquired  cases'.    Ataxic  Paraplegia  of  Cowers. 

Etiology. — Occurs  in  males  chiefly,  between  thirty  and  forty 
years  of  life.  Not. after  syphilis,  but  after  exposure  to  cold  or 
sexual  excess.     Possibly  after  concussion  of  spine. 

Symptoms. — Slow  onset  of  weakness  and  ataxia  together. 
Undue  fatigue,  unsteady  gait.  Romberg  symptom.  Dull  pain  in 
back  and  legs,  no  lightning  pains.  Reflexes  increased.  Knee- 
jerk  high,  ankle  clonus  present.  Sexual  power  lost.  Sphincters 
less  impaired  than  in  tabes.  Eye  symptoms  very  rare.  Tremor 
of  face  and  speech  sometimes  develops. 

Differs  from  tabes  in  fact  that  the  nerve-roots  are  not  in- 
volved. 


DISEASES    OF   THE    NERVOUS    SYSTEM.  41 

Course. — Weakness  increases  slowly  to  paralysis.  Rigidity 
soon  develops,  and  contractures.  Death  occurs  from  complica- 
tions. 

The  Association  Columns. 

8.  Antcro-Latcval  Coliiiiin. — There  is  a  large  collection  of 
nerve-fibres  forming  a  white  column  lying  adjacent  to  the  gray 
matter  of  the  cord,  in  front  and  inside  of  the  pyramidal  tract,  and 
inside  of  the  direct  cerebellar  and  antero-lateral  ascending  tracts, 
extending  as  far  forward  as  the  anterior,  nerve-roots.  (See  Fig. 
1.)  A  portion  lying  next  to  the  gray  matter  has  been  named  the- 
lateral  liinitiJig  layer.  This  column  contains  a  few  fibres,  which 
degenerate  all  the  way  upward  to  the  medulla,  and  it  is  possible 
that  some  sensory  impulses  are  transmitted  through  it.  (See  Fig. 
9. )  The  major  part  of  the  fibres  are,  however,  short,  and  serve 
to  connect  the  various  segments  of  the  cord  with  one  another. 
(See  Fig.  8.  )  In  it  pass  the  majority  of  the  "association  fibres" 
of  the  cord,  which  harmonize  the  action  of  different  parts. 

g.  Anterior  Column. — This  lies  between  the  exit  of  the  an- 
terior nerve-roots  and  the  anterior  median  column.  It  has  the 
same  function  as  the  antero-lateral  column,  and  like  it  ends  in  the 
formatio  reticularis  of  the  medulla. 

There  are  very  many  polygonal  cells  scattered  through  the 
gray  matter  in  both  horns  and  in  the  central  gray  which  send  out 
to  these  columns  an  axis-cylinder  process,  which  on  entering  the 
column  bifurcates,  sending  one  branch  down  and  the  other  up- 
ward. These  branches  give  off  collaterals  in  their  course,  which 
pass  into  the  gray  matter  at  various  levels  and  terminate  in  brush- 
like expansions.  The  original  branches  terminate  in  the  same  way 
after  having  a  longer  or  shorter  course.  Thus  the  majority  of 
the  fibres  in  these  columns  are  true  association  fibres.  There  are 
a  few  such  fibres  also  in  the  portion  of  the  posterior  columns 
adjacent  to  the  gray  commissure. 

Secondary  Degenerations. 

When  the  cord  is  divided  by  an  injury  or  by  transverse  mye- 
litis there  results  a  defeneration  in  the  various  columns. 


4a  DISEASES    OF   THE    NERVOUS    SYSTEM. 

The  anterior  median  and  lateral  pyramidal  columns  degen- 
erate downward  for  their  entire  length.  There  is  also  a  short 
tract  of  degeneration  downward  in  the  lateral  zone  of  the  column 
of  Burdach.  The  anterior  and  antero-lateral  columns  degenerate 
downward  for  a  short  distance. 

The  columns  of  Burdach  and  Goll  and  Gowers  and  the  direct 
cerebellar  column  degenerate  upward  through  their  entire  length. 
The  columns  of  Lissauer,  and  the  anterior  and  antero-lateral  col- 
umns degenerate  upward  for  a  short  distance. 

Such  degenerations  are  due  to  the  fact  that  the  transverse 
lesion  cuts  ojff  the  individual  fibres  from  their  nutrient  cells,  and 
hence  the  distal  end  degenerates,  the  fibres  nourished  by  cells 
above  the  lesion  degenerating  downward  and  those  by  cells  below 
the  lesion  degenerating  upward. 

]\Iyelitis. 

This  is  an  inflammation  or  softening  of  the  spinal  cord  in- 
volving an  entire  segment,  both  gray  and  white  matter. 

Pathology. — Cord  looks  normal,  but  feels  soft  at  points ;  or 
may  break  in  two  and  be  soft  enough  to  be  fluid.  On  cutting  it 
the  cut  surface  swells  out  as  if  semifluid ;  the  gray  matter  looks 
red  and  capillary  hemorrhages  are  seen ;  the  limit  of  white  and 
gray  is  indistinct. 

Microscopically. — Large  numbers  of  inflammatory  corpuscles 
everywhere.  Nerve-cells  and  fibres  swollen  and  degenerated, 
granular  and  disappearing  or  atrophied.  Neuroglia  cells  in- 
creased. Deiter's  spider  cells  present.  Fatty  and  granular  cells 
■everywhere  as  evidence  of  degeneration.  Vessels  are  distended 
with  blood  and  ruptured ;  walls  ma}^  be  infiltrated  and  thickened. 

Secondary  degenerations  as  already  enumerated. 

Etiology. — Males  more  than  females.  Soldiers,  porters. 
Age,  ten  to  forty.  Exposure  to  cold.  Overexertion.  Falls  and 
blows.  Concussion  of  cord.  Sexual  excesses.  Menstrual  sup- 
pression. After  confinement.  Injuries  of  the  cord.  Compres- 
sion of  the  cord  by  disease  of  spinal  bones  or  tumors.  Secondary 
to   acute   infectious    diseases.      Syphilis   and   chronic   alcoholism, 


DISEASES    OE     IKE    XER\'OUS    SVSTEM.  43 

often  due  to  honiorrhao^e  or  to  thrombosis  in  diseased  vessels, 
"spinal  apoplexy." 

Varieties.  General. — Entire  cord  affected — ascending  or  de- 
scending. 

Disseiiiiitafed. — X'arious  segments  at  different  levels  affected. 

Traiisz'ersc. — One  or  two  segments  at  one  level  aft'ected. 

Syinptoms. —  (i)  Direct,  due  to  destruction  of  cord  tissue. 

I.  ^Nlotor.  Paralysis,  atrophy.  R.  D.  Loss  of  tone  in  mus- 
cles. 

•^.  Reflex.  Loss  of  spinal  reflexes.  Paralysis  of  the 
bladder  and  rectum,   impotence 

3.  Sensory.  Xumbness.  Pain.  Parjesthesia,  ansethesia. 
Hypersesthesia  at  upper  level  of  lesion.  Pain  and  tenderness  of 
back  to  heat. 

4.  A'asomotor  and  trophic.  Lnperfect  circulation.  Skin 
cold.     Sweat  profuse.     Bedsores  on  buttocks,  sacrum,  and  heels. 

The  distribution  of  the  direct  symptoms  depends  on  the  ex- 
tent of  the  lesion.  If  general  they  are  universal.  If  disseminated 
they  are  scattered.     If  transverse  they  are  limited  to  one  level. 

Diagnosis  of  level  from  situation  of  symptoms,  motor  or 
sensory,  see  table,  page  14. 

Syiiipfoius. —  (2)  Indirect,  due  to  cutting  off'  of  impulses  to 
other  parts.  The  cord  transmits  impulses  to  and  from  the  brain. 
In  disseminated  and  transverse  myelitis  tracts  are  broken,  (i) 
Motor  tracts  to  parts  below,  hence  secondary  lateral  sclerosis 
with  its  symptoms.  (2)  Sensory  tracts  from  parts  below,  hence 
secondary  degenerations   upward   with   their   symptoms. 

Secondary  symptoms  are : 

1.  Rigidity  and  increased  reflexes,  contractures,  spasms  of 
legs,  paralyzed  muscles  not  atrophied,  and  no  R.  D. 

2.  Loss  of  bladder  control  without  bladder  paralysis,  priap- 
ism. 

3.  Imperfect  sensation  without  incoordination. 

4.  Imperfect  perception  of  pain  ;  hence  bedsores  from  dirt, 
bedsores  over  sacrum,  glutei,  heels,  and  ankles. 

Examples  :  In  general  myelitis,  direct  symptoms  throughout 
bodv. 


44  DISEASES    OF    THE    NERVOUS    SYSTEM. 

In  disseminated  myelitis,  direct  symptoms  in  irregular  areas, 
few  indirect  symptoms. 

In  transverse  myelitis,  direct  symptoms  very  limited,  in- 
direct symptoms  below  the  lesion.  • 

(a)  Cervical  transverse  myelitis,  direct  symptoms  in  arms, 
indirect  in  legs. 

(b)  Dorsal  transvere  myelitis,  direct  symptoms  few,  in  trunk, 
indirect  in  legs  like  lateral  sclerosis,  arms  free. 

(c)  Lumbar  transverse  myelitis,  direct  symptoms  in  legs, 
arms  free,  no  indirect  symptoms. 

Course  of  General  Myelitis  and  Disseminated  Myelitis. — ■ 
Aciite  or  subacute,  onset  in  two  weeks  after  a  cold  or  great  strain 
or  after  typhus,  typhoid,  small-ppx,  confinement,  syphilis.  Weak- 
ness in  limbs.  Pains  in  back  and  limbs.  Prostration.  Then 
paralysis.  Pain  and  anaesthesia.  Bladder  and  rectal  symptoms. 
Then  patient  is  confined  to  bed  and  bedsores  develop.  Slow 
course  for  a  year  to  three  years  and  occasionally  gradual,  im- 
perfect recovery.  Usually  cystitis,  bedsores,  or  'pneumonia  and 
death. 

Course  of  Transverse  Myelitis. — Acute,  onset  after  injury — 
blow,  fall,  wound,  dislocation  of  spine,  or  strain,  causing  hem- 
orrhage in  cord ;  or  from  embolism  of  spinal  arteries. 

Chronic,  onset  after  spinal  caries  with  deformity  and  pres- 
sure, or  tumor  in  spinal  canal  or  cord.  Course  depends  on  possi- 
bility of  removing  the  cause. 

Diagnosis. — ]\Iyelitis  z's.  multiple  neuritis,  see  page  11. 

Myelitis  vs.  IMexixgitis. 

Very  rapid  onset.  Slower  onset. 

Fever  moderate.  Fever  high. 

Pain  in  back  moderate,  in  limbs  or         Pain    in   back   and   body    and   limbs 

body  dull.  very  severe,  increased  by  motion. 

Hyperjesthesia    slight    in    a  band   at     Hyperesthesia    of    entire    body    and 

upper  level  ol  lesion.  limbs  very  intense. 

Anaesthesia  below  lesion.  No  anaesthesia. 

No  spasms  or  rigidity.  Spasms    of    limbs    and    back    with 

rigidity  of  back  appear  early. 

Paralysis     total     in     some  muscles     Paralysis  only  apparent ;  due  to  fear 

with  atrophy  and  R.  D.  of  pain  on  motion,  no  atrophy. 

Sphincters  paralyzed.  Sphincters  not  affected. 

Bedsores  and  cvstitis.  No  bedsores  or  cystitis. 


DISEASES    OF   THE    NERVOUS    SVS'l'E.M.  45 

]Myelitis  t's.  Hysterical  Parai'legia. 

Anaestliesia     below     lesion     includes  Anaesthesia  varies  in  level  and  geni- 

genitals.  tals  never  included. 

If       thighs       are       paralyzed       and  When    legs    are    paralyzed    reflexes 

atrophied  reflexes  are  lost.  are  exaggerated. 

Usually   some   muscles   atrophj'   and  Muscles    rarely   atrophy   and    R.    D. 

show  R.  D.  never  appears. 

Sphincters  usually  involved.  Sphincters  rarely  involved. 

Diagnosis  of  level  of  lesion  by  distribution  of  anaesthesia,  see 
table,  page  14. 

Treatment  of  myelitis. 

When  onset  is  acute  remove  cause,  and  use  counter-irritation, 
ice-bag.  or  warm  douche.  Keep  at  perfect  rest  in  prone  position. 
Give  sedatives  and  ergot :  in  early  stage  give  purgatives,  calomel, 
or  salts. 

^^'hen  case  is  chronic  in  onset  or  in  cours'e  :  employ  counter- 
irritation.  Cups,  blisters,  cautery,  ether  spray ;  but  not  in  cases 
with  tendency  to  bedsores.  Use  baths,  douches,  tepid  and  cold, 
to  spine.  Keep  up  strength  of  patient  by  good  diet,  and  regulate 
digestion.  Use  massage  to  the  limbs — hot  baths  for  rigidity.  Use 
interrupted  galvanic  current  to  atrophied  and  paralyzed  muscles. 

Prevent  cystitis  by  keeping  catheters  and  parts  clean  and 
aseptic. 

Treat  cystitis  by  washing  out  the  bladder,  as  in  surgery. 

Prevent  bedsores  by  careftil  padding  or  water-bed,  by  spong- 
ing with  alcohol  and  alum-water,  by  frecj[uent  change  of  position. 

Treat  bedsores  by  aseptic  dressings,  as  in  surgery. 

For  pain,  apply  heat  or  faradic  brush  to  part.  Give  antipyrin, 
antifebrin,  phenacetine,  morphine,  salicin,  salicylic  acid. 

For  spasms,  apply  heat  to  spine,  or  hot  bath  to  legs,  or  cups. 
Give  bromides.     For  rigidity,  when  beginning,  pads  and  massage. 

For  incontinence  of  urine,  pads  of  absorbent  cotton,  or  wear 
urinal. 

Medicines  in  chronic  myelitis :  Iodide  of  potash,  gr.  x.  to 
XX.,  t.i.d.  Xitrate  of  silver  in  pill  with  kaolin,  gr.  1-4  t.i.d.  in- 
creased. Ergotin  when  congestion  is  suspected.  Strychnine 
when  an  increase  of  reflex  activity  is  not  present.  Phosphorus 
and  arsenic  as  nerve  tonics.  Use  ung.  hydrarg.  and  KI  in  large 
doses  in  syphilitic  cases. 


46 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


Hemorrhage  into  the  Spinal  Cord. 


Hemorrhage  into  the  spinal  cord 
or  into  the  membranes  is  a  rare  oc- 
currence, and  is  ahnost  always  due 
to  traumatism.  The  symptoms  pro- 
duced are  those  of  sudden  suspension 
of  all  spinal  functions  at  and  below 
the  level  of  the  hemorrhage.  They 
are  therefore  identical  with  those  of 
transverse  myelitis,  and  the  sudden 
onset  affords  the  only  means  of  dis- 
tinguishing the  two  diseases.  Some- 
times spontaneous  hemorrhages  in 
the  anterior  horn  cause  symptoms  of 
anterior  poliomyelitis.  Sometimes 
central  hemorrhages  cause  symptoms 
of  syringomyelitis. 

Tumors  of  the  Spinal  Cord. 

Tumors  rarely  grow  in  the  spinal 
cord.  They  are  usually  secondary 
to  tumors  elsewhere.  All  varieties 
may  occur.  The  symptoms  produced 
are  those  of  transverse  myelitis  of 
slow  onset  and  characterized  by  ex- 
treme pain  at  the  level  of  the  tumor 
or  in  the  sensory  areas  which  corre- 
spond to  the  segment  in  which  the 
tumor  grows.  The  only  relief  is  by 
operation.  The  relation  of  the  seg- 
ments of  the  cord  to  the  spinal  col- 
umn is  shown  in  Fig.  11. 

Brown-Sequard's   Paralysis. 

Hemorrhages  in  the  cord,  tumors 
in  or  about  the  cord,  and  bony 
growths  or  callus,  the  result  of 
injury,    sometimes    divide    or    com- 


FiG.  II. — Relations  between  the  Segments 
of  the  Spinal  Cord  and  their  Nerves  and 
the  Bodies  of  the  Vertebrae.     (Gowers.) 


.  DISEASES    OF   THE    NERVOUS    SYSTEM.  47 

press  one-half  only  of  tlie  cord.  The  symptoms  resulting- 
were  first  described  by  Brown-Sequard,  and  hence  the  condi- 
tion has  been  named  after  him.  This  condition  is  as  follows  : 
(i)  on  the  side  of  the  lesion  there  is  paralysis  with  increased 
reflexes,  and  sometimes  a  loss  of  muscular  sense  below  the  level 
affected,  and  a  marked  hypersesthesia  to  touch  and  pain;  (2)  on 
the  side  opposite  to  the  lesion  there  is  no  paralysis,  but  there  is 
a  loss  of  sensation  of  touch,  temperature,  and  pain,  and  some- 
times a  development  of  bedsores  below  the  level  of  the  lesion  ; 
(3)  at  the  level  of  the  lesion  there  is  a  band  about  the  body  of 
anaesthesia  ,with  another  band  of  hyperaesthesia  above  it;  the 
band  on  the  side  of  the  lesion  being  a  little  higher  than  upon 
the  opposite  side. 


THE  BRAIN  AND   ITS   DISEASES. 


I.  The  Cortex  of  the  Cerebral  Hemispheres. 

The  cortex  consists  of  gray  matter  spread  out  in  a  layer  over 
the  cerebral  hemispheres,  3mm.  thick  and  about  200,000  sq.  mm. 
in  extent ;  its  amount  varying  greatly  in  different  persons ;  its 
development  determining  mental  capacity.  The  development  of 
fissures  throwing  the  cortex  into  folds  enables  this  large  extent 
to  be  contained  in  the  skull. 

The  Microscopic  Appearance  of  the  Cortex. — Cells  arranged 
in  layers. 

(1)  Superficial  or  molecular  layer  J^-  small  cells.  Much 
neuroglia. 

(2)  Layer  of  small  pyramids  -^^  with  many  branches  and 
short  process. 

(3)  Layer  of  large  pyramids  /q  with  few  branches  and 
a  long  projection-fibre  process. 

(4)  Layer  of  polymorphous  cells  fg-  with  many  short 
branches  and  a  short  process. 

(5)  '  Layer  of  fusiform  cells  /„  with  short  branches  and 
association-fibre  process. 

Fibres  trasverse  these  layers,  giving  off  collaterals,  and 
form  an  intricate  network  throughout  the  gray  matter.  There  are 
great  variations  in  the  structure  of  different  regions.  (See 
"Quain's  Anatomy,"  loth  Ed.,  Vol.  III.  Starr's  "Atlas  of  Nerve 
Cells.") 

The  fibres  arising  from  the  cortex  and  constituting  the  white 
matter  beneath  it  are  ( i )  association  fibres  passing  to  some  other 
part  of  the  cortex;  (2)  commissural  fibres  passing  to  the  cortex 
of  the  opposite  hemisphere;  (3)  projection  fibres  passing  to  the 
basal  ganglia,  cerebral  axis,  or  spinal  cord. 

Divisions    of    the    Cortex    into    Lobes    and    Convolutions. — 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


49 


Frontal  lobe,  40  per  cent. ;  parietal  lobe,  20  per  cent. ;  temporal 
lobe,  20  per  cent.;  occipital  lobe,  17  per  cent.;  Island  of  Reil,  3 
per  cent,  of  extent  of  cortex. 

Landmarks  on  the  Cortex. — Fissure  of  Sylvius,  fissure  of 
Rolando,  interparietal  fissure,  parieto-occipital  sulcus,  calcarine 
fissure,  callosomarginal  fissure. 

C<li.\  N  lO-CCRIiURAL    Toi'OCRAPII  V. 

To  find  the  fissure  of  Rolando,  lay  down  a  line  from  the  root 
of  the  nose  to  the  occipital  protuberance  over  the  top  of  the  head 
and  take  a  point  0.557  of  the  distance  back  upon  this  line.     This 


df'sfan 


Ccclp 
pmu~ 


Glahella 


Fig.    12. 


point  will  correspond  to  the  upper  end  of  the  fissure.  The  fis- 
sure makes  an  angle  of  67°  with  the  median  line  just  measured. 
Hence  if  two  strips  of  metal,  fixed  to  one  another  at  this  angle, 
be  placed  on  the  head  with  their  junction  upon  the  upper  end  of 
the  fissure,  when  one  strip  is  on  the  median  line  the  other  strip, 
pointing   forward  and   downward,   must   lie   over  the   fissure  of 


50  DISEASES    OF   THE    NERVOUS    SYSTEM. 

Rolando.  In  its  lower  third  the  fissure  becomes  a  little  more  ver- 
tical than  the  strip.  The  fissure  is  about  three  and  a  half  inches 
long. 

To  find  the  fissure  of  Sylvius,  la}^  down  a  base  line  from 
the  lower  margin  of  the  orbit  to  the  auditory  meatus.  Lay  down 
a  second  line  parallel  to  the  base  line  from  the  external  angular 
process  of  the  frontal  bone  backward  one  inch  and  a  quarter,  and 
then  measure  upward  one-quarter  of  an  inch ;  this  gives  point 
one.  Fnd  the  most  prominent  part  of  the  parietal  eminence  and 
from  it  draw  a  line  downward  perpendicular  to  the  base  line,  and 
on  this  take  a  point  three-quarters  of  an  inch  below  the  eminence ; 
this  gives  point  two.  Join  these  two  points,  and  the  line  will  lie 
over  the  fissure  of  Sylvius.  The  anterior  limb  of  the  fissure  will 
be  two  inches  behind  the  external  angular  process.  The  fissure 
of  Sylvius  is  about  four  inches  long. 

To  find  the  parieto-occipital  fissure,  continue  the  line  of  the 
fissure  of  Sylvius  to  the  median  line.  At  their  junction  lies  this 
fissure.  Since  all  areas  now  open  to  surgical  operation  can  be 
located  with  a  definite  relation  to  these  fissures,  no  further  rules 
are  necessary.  Since  in  opening  the  skull  it  is  customary  to  make 
a  fenestra  of  at  least  an  inch  in  diameter,  and  it  is  frequently 
necessary  to  enlarge  the  opening  much  more,  a  procedure  in  no 
way  dangerous  under  aseptic  conditions,  there  is  no  difficulty 
in  recognizing  the  fissures  and  convolutions  exposed  if  the  rules 
are  closely  followed.  Prior  to  the  large  incision  of  the  scalp  it  is 
well  to  mark  certain  points  upon  the  skull  by  the  sharp  point  of  a 
chisel,  so  that  when  the  bone  is  laid  bare  surface  landmarks  may 
still  be  kept  in  view. 

Localization  of  Functions  in  the  Cortex. 

Proofs  from  comparative  anatomy ;  natural  and  experimental 
atrophy ;  process  of  development ;  irritation  and  excision  of  cortex 
with  various  results ;  pathological  lesions  of  limited  extent  with 
secondary  degenerations. 

The  functions  of  the  cortex  in  general  are : 

(i)  To  receive  impressions  from  the  various  sensory  organs 
as  conscious  perceptions. 


DISEASES    OF    THE    NERVOUS    SYSTEM.  51 

(2)  To  associate  these  various  simultaneous  perceptions  in- 
to a  mental  image  or  concept. 

(3)  To  retain  these  concepts  as  memories  so  that  objects  can 
be  recognized  or  recalled. 

(4)  To  give  expression  to  thought  in  action  and  in  speech. 

(5)  To  restrain  the  flow  of  thought  and  to  inhibit  or  control 
automatic  and  reflex  acts. 

It  has  been  established  that  various  powers  of  perception, 
memory,  and  volition  can  be  definitely  assigned  to  various  parts 
of  the  brain;  that  each  sense  has  its  corresponding  area  in  the 
cortex,  and  each  voluntary  movement  its  point  of  departure  from 
the  cortex. 

It  has  been  proven  that  perceptions  leave  behind  them  a  phys- 
ical trace  inseparably  connected  with  the  area  in  which  they 
were  originally  received;  that  irritation  of  this  area  produces  a 
renewal  in  consciousness  of  the  original  perception  as  a  memory, 
which  may  be  so  vivid  as  to  appear  real,  being  then  an  hallucina- 
tion ;  that  destruction  of  this  area  causes  a  loss  of  the  power  of  re- 
calling the  previous  perception  or  of  recognizing  it  when  repeated. 

It  has  been  proven  that  movements  which  are  acquired  by 
practice,  and  are  therefore  the  result  of  conscious  effort,  are  al- 
ways initiated  from  a  definite  area ;  that  this  area  is  inseparably 
related  to  movements ;  since  its  irritation,  b}-  any  cause,  results  in 
the  production  of  forcible  movements  of  the  nature  of  spasms, 
and  its  destruction  produces  a  loss  of  the  power  of  movement  or 
paralysis  of  voluntary  action. 

It  has  been  proven  that  the  use  of  language  involves  both  the 
recollection  of  auditory  and  visual  symbols  and  the  initiation  of 
impulses  of  speech  and  writing,  thus  calling  into  play  not  only  the 
motor  portion  of  the  brain,  destruction  of  which  therefore  causes 
a  loss  of  speech,  but  also  the  sensory  portion  of  the  brain,  a  lesion 
of  which  will  also  cause  aphasia. 

There  are  certain  areas  upon  the  cortex  of  the  brain,  not 
necessarily  coextensive  with  either  lobes  or  convolutions,  whose 
functions  are  accurately  known. 

These  areas  are:  (i)  The  sensori-motor  area.  (2)  The 
visual  area.  (3)  The  auditory  area.  (4)  The  area  of  sensations 
of  smell  and  of  taste.     (5)  The  speech  areas. 


52 


DISEASES    OF    THE    NERVOUS    SYSTEM. 


Fig.  13. — Diagram  of  the  Fissures  and  Convolutions  of  the  Convexity  of  the  Left 
Hemisphere  of  the  Brain,  with  the  areas  presiding  over  various  functions.  The 
speech  areas  are  shown  on  this  hemisphere.  The  motor  area  is  more  extensive  on 
the  left  than   on  the  right  hemisphere. 


The  Sensori-Motor  Area. 


The  scnsori-inotor  area  includes  the  cortex  of  the  anterior 
and  posterior  central  convolutions  which  border  the  fissure  of  Ro- 
lando and  the  adjacent  cortex  in  front  and  behind  these  convolu- 
tions. Each  hemisphere  controls  movement  on  the  opposite  side 
of  the  body,  but  as  the  right  hand  is  more  generally  used  and  is 
better  trained  than  the  left,  this  area  is  larger  on  the  left  hemi- 
sphere than  on  the  right. 

The  cortex  of  the  posterior  part  of  the  second  frontal  convo- 
lution controls  the  movements  of  the  eyes  and  head.  Impulses 
starting  from  this  area  produce  conjugate  movement  of  these 
parts  toward  the  opposite  side.  The  eye  district  is.  below,  the 
head  district  above. 

The  lower  third  of  the  anterior  and  posterior  central  convolu- 
tions governs  the  movements  of  the  face,  tongue,  larynx,  and 
pharynx.  The  eyebrows  and  cheeks  are  controlled  by  the  upper 
and  forward  part  of  this  area ;  the  tongue  and  larynx  by  the  lower 


DISEASES    OF   THE    NERVOUS    SYSTEM.  53 

and  forward  part :  the  mouth,  pliarynx,  and  platysnia  by  the  hinder 
part. 

The  middle  third  of  the  anterior  and  posterior  central  convo- 
lutions governs  the  movements  of  the  upper  extremity ;  the 
shoulder  motions  being  controlled  in  the  anterior  and  upper  part 
of  this  area,  the  elbow  motions  in  its  middle  part,  and  the  h.and 
and  finger  motions  in  its  posterior  and  lower  part. 

The  upper  third  of  the  anterior  and  posterior  central  convo- 
lutions, including  their  junction  in  the  paracentral  lobule,  con- 
trols the  motions  of  the  lower  extremity,  the  thigh,  knee,  foot,. 
and  toes  being  governed  by  various  parts  of  this  area  from  before 
backward  in  the  order  named. 

The  parts  susceptible  of  the  finest  and  most  delicate  move- 
ments, those  directed  by  the  most  acute  sensations,  the  lips,  the 
fingers,  and  the  toes,  lie  furthest  back  in  the  motor  area,  in  the 
depth  of  the  fissure  of  Rolando  and  in  the  posterior  central  con- 
volution. Lesions  in  this  convolution  almost  always  cause  some 
loss  of  tactile  sensation  as  well  as  paralysis,  and  hence  this  area 
is  thought  to  be  the  seat  of  tactile  sensations  as  well  of  move- 
ments, while  some  cases  point  to  the  localization  of  muscular  sen- 
sations in  the  area  just  behind  that  of  motion. 

The  trunk  or  body  motor  centres  lie  between  those  of  the  leg 
and  arm. 

There  are  no  sharply  defined  sections  of  the  motor  area  to  be 
assigned  to  special  motions.  Each  motion,  each  part  of  a  limb. 
has  a  wide  general  representation  over  the  cortex  and  a  special 
representation  at  a  limited  area.  The  areas  of  representation  of 
different  limbs  merge  into  one  another  ;  thus,  in  the  representa- 
tion of  the  thumb  we  find  that  there  is  a  focus,  but  that  the  thumb 
is  represented  over  a  great  deal  of  the  upper  limb  region,  and  that 
this  representation  diminishes  in  intensity  gradually  as  we  pass 
from  the  focus  upward.  This  explains  the  fact  that  the  excision 
of  a  small  area  does  not  totally  paralyze  the  portion  of  the  limb 
represented  chiefly  on  that  area.  The  adjacent  areas  represent  to 
some  extent  that  limb,  and  hence  can  govern  it  if  need  be. 

The  motor  centres  govern  motor  acts  rather  than  special 
muscles,  each  act  involving  a  succession  of  movements  of  differ- 
ent joints  by  various  groups  of  muscles. 


54  DISEASES    OF    THE    NERVOUS    SYSTEM. 

Cortical  Spas)n  and  Paralysis. — Irritation  in  the  motor  area 
produced  by  any  kind  of  disease  gives  rise  to  localized  spasms  or 
convulsions,  called  Jacksonian  epilepsy.  Destruction  of  the  motor 
area  gives  ries  to  paralysis.  The  point  of  beginning  of  the  spasm 
or  the  extent  of  paralysis  depends  on  the  part  of  the  motor  area 
diseased.  Hence,  from  the  character  of  either  of  these  symptoms 
a  conclusion  can  be  reached  as  to  the  location  of  the  disease.  Cor- 
tical spasm  or  paralysis  usually  begins  in  the  face  or  in  one  limb 
of  one  side  and  extends.  The  order  of  the  progress  also  indicates 
the  location  of  the  disease,  e.  g.,  from  face  to  arm,  then  to  leg; 
or  vice  versa,  e.  g.,  spasm  of  shoulder,  arm,  and  hand,  vs.  spasm 
of  fingers,  arm,  and  shoulder :  the  disease  is  most  intense  in  the 
part  first  affected.  Sensations  of  numbness  precede  the  spasm. 
A  cortical  spasm  begins  locally,  and  usually  extends  until  one 
side  of  the  body  is  affected.  It  is  usually  followed  by  temporary 
weakness.    Consciousness  is  preserved. 

Cortical  paralysis  is  monoplegic  in  type  vs.  subcortical  par- 
alysis, which  is  hemiplegic  in  type.  A  slowly  advancing  paralysis 
indicates  a  slowly  extending  destruction  of  tissue.  Cortical  par- 
alysis is  associated  with  increased  reflexes,  but  there  is  no  atrophy 
and  no  change  in  electric  reactions.     Contractures  develop  late. 

The  Visual  Area. 

The  area  of  sensations  of  sight  is  located  in  the  occipital  lobe 
of  the  brain,  including  the  cuneus  on  the  median  surface  and  the 
occipital  convolutions  on  the  convexity.  The  cortex  lying  in  the 
calcarine  fissure  is  the  part  primarily  reached  by  the  visual  im- 
pulses, but  the  parts  named  are  also  concerned  in  vision.  Each 
occipital  lobe  receives  impressions  from  one-half  of  both  eyes ; 
hence  a  lesion  in  one  lobe  produces  hemianopsia,  a  half-blindness 
in  both  eyes,  the  blind  field  of  vision  being  on  the  opposite  side  to 
the  lesion.  This  is  termed  homonymous  hemianopsia ;  that  is, 
a  blindness  in  the  like-named  halves  of  both  visual  fields.  When 
the  right  occipital  lobe  is  affected,  the  patient  cannot  see  anything 
on  the  left  side  of  the  middle  line  as  he  looks  forward. 


-V-w 


z 


V-tAi) 


DISEASES    OF    THE    NERVOUS    SYSTEM. 


Fig.  14.— The  \'isual  Tract.  The  result  of  a  lesion  anywhere  between  the  chiasm  and 
cuneus  is  to  cause  homonyrnous  hemianopsia.  III.  Third  nerve;  S.  N.,  substantia 
nigra;  R.  N.,  red  nucleus  of  tegmentum;  L.,  lemniscus;  T.  G.,  fibres  from  optic 
tract  to  corpora   quadrigemina. 

Irritation  of  the  occipital  lobe  may  cause  hallucinations  of 
light  or  even  of  objects  which  are  referred  to  the  opposite  visual 


56  DISEASES    OF    THE    NERVOUS    SYSTEM. 

field.  Destruction  of  the  occipital  lobe  on  the  left  side  destroys 
sight-memory  pictures ;  hence  recognition  of  things  seen  may  be 
impossible,  and  reading  power  may  be  lost. 

The  Auditory  Area. 

The  area  of  sensations  of  sound  is  located  in  the  first  and 
second  temporal  convolutions  of  the  brain.  Each  ear  is  connected 
with  both  hemispheres  ;  hence  deafness  from  a  unilateral  lesion  is 
only  partial  and  is  not  generally  noticed.  But  if  both  temporal 
lobes  are  destroyed  the  patient  becomes  totally  deaf.  Irritation 
of  the  temporal  cortex  may  cause  hallucinations  of  hearing.  This 
may  be  the  first  symptom  of  a  convulsion  whose  origin  is  an  irri- 
tation in  this  part  of  the  cortex.  Destruction  of  the  temporal  cor- 
tex on  the  left  side  causes  word-deafness.     (See  speech  areas.) 

The  Smell  and  Taste  Area. 

The  area  of  sensations  of  smell  and  taste  is  located  at  the  tig^ 
,of  the  temporal  lobe  on  its  under  and  inner  surface,  which  rests 
on  the  sphenoid  bone.  Each  lobe  is  related  to  sensory  organs  on 
both  sides,  and  unilateral  lesion  does  not  often  produce  noticeable 
symptoms. 

The  Speech  Areas  and  Aphasl\. 

The  speech  areas  are  of  four  kinds  and  in  four  locations. 
They  are  limited  to  the  left  hemisphere  in  right-handed  persons 
and  to  the  right  hemisphere  in  left-handed  persons.  There  is 
the  motor-speech  area  in  the  posterior  part  of  the  third  frontal 
convolution  (Broca's  convolution),  in  which  the  movements  con- 
cerned in  the  act  of  speaking  are  controlled.  The  use  of  language 
and  the  power  of  talking  are  affected  when  this  region  is  de- 
stroyed. There  is  the  andijory-jpccch  area  in  the  first  and  second 
temporal  convolutions,  in  which  the  memories  of  word-sounds 
are  stored  up.  The  understanding  of  language  and  the  power 
of  recollecting  the  names  of  objects  are  lost  when  this  region  is 
destroyed.  There  is  the  visual-speech  area  in  the  ocdp^ital  and 
lower  parietal  region.,  in  which  th.e  memories  of  printed  words 


iyl/t-^ 


DISEASES    OF    THE    NERVOUS    SYSTEM. 


57 


arc  stored  up.  The  untlerstanding  of  written  language  and  the 
power  to  read  are  lost  when  this  region  is  destroyed.  The  pozver 
of  zcriting  is  a  part  of  speech  and  is  usually  lost  when  the  motor- 
speech  area  is  destroyed,  but  its  exact  location  is  not  fully  deter- 
mined ;  some  cases  pointing  to  the  second  frontal  convolution, 
others  to  the  lower  parietal  convolution  near  the  hand  centre  as  its 
probable  cortical  position.     (See  Fig.  15.) 

It  is  accepted  that  every  word  in  ordinary  use  has  a  complex 
mental  substratum,  which  may  be  termed  the  word-image,  made 
up  of  a  number  of  memory  pictures.  The  memory  of  the  sound  of 
a  word  as  spoken,  the  memory  of  the  appearance  of  the  word  as 
printed,  the  memory  of  the  muscular  movements  needed  to  write 
the  word  or  to  pronounce  it,  are  known  to  be  distinct  from  one 
another  and  yet  to  be  associated  together.     Loss  of  one  of  these 


Hand 


Touch 


Hearing 


Fig.  15. — Diagram  to  illustrate  Aphasia.  The  cortical  sensory  and  motor  centres 
are  indicated  by  arrows.  The  secondary  cortical  centres  of  memories  are  indicated 
by  circles.  I.  Visual  of  Objects.  II.  Visual  of  Words.  III.  Tactile.  IV. 
Auditory.  \'.  Speech.  \l.  Writing.  These  are  joined  to  each  other  by  association 
fibres  which  send  impulses  in  both  directions.  Lesions  of  the  association  fibres 
as  well  as  lesions  of  the  cortex  cause  aphasia. 


-"58 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


memory-pictures,  or  disturbance  in  their. association,  impairs  the 
integrity  of  the  word-image,  and  produces  such  defects  in  its  use 
as  are  indicated  by  the  names  given  to  the  respective  varieties  of 
aphasia.  A  division  of  disturbances  of  speech  has  been  made 
into  two  great  classes  of  sensory  and  motor  aphasia — the  first  due 
to  defect  in  the  receptive,  and  the  second  due  to  impairment  of  the 
emissive  functions  of  the  brain.  A  further  subdivision  into  sev- 
eral varieties  has  been  made.  These  are  word-deafness,  word- 
blindness,  agraphia,  motor  aphasia,  and  paraphasia.  But,  before 
considering  these  defects,  let  us  look  at  the  physical  basis  of  the 
thought  which  lies  back  of  the  wor.  Take  the  concept  "bell"  as 
an  example. 


Fig.    i6. 


The  concept  of  a  bell  is  made  up  of  separate  memory-pictures 
of  its  shape,  size,  color  (visual-picture)  ;  weight  (muscular-sense 
picture)  ;  cold  smooth  surface  (touch-picture)  ;  and  sound  (audi- 
tory-picture). These  various  memories,  received  by  different 
senses  and  stored  up  in  different  parts  of  the  cortex,  are  associated 
together  in  a  mental  image  of  the  object  bell. 


DISEASES    OF   THE    NERVOUS    SYSTEM.  59 

To  this  mental  ima^c  the  word-image  is  added  of  the  word 
bell  as  heard,  as  printed,  as  spoken,  as  written,  making  up  a  eon- 
geries  of  memory-pictures  forming  a  "concept."  Any  one  of 
these  memory-pictures  may  be  lost  by  disease.  If  the  memories 
of  the  object  are  lost  the  symptom  is  called  apraxia.  If  the  memo- 
ries of  the  word  are  lost  the  symptom  is  called  aphasia. 

To  examine  an  aphasic  thoroughly  it  is  necessary  to  test — 

1.  The  power  to  recognize  objects  seen,  heard,  felt,  tasted, 
or  smelt,  and  their  use. 

This  will  determine  whether  the  condition  of  apraxia  is 
present. 

2.  The  power  to  recall  the  spoken  name  of  objects  seen, 
heard,  handled,  tasted,  or  smelt. 

3.  The  power  to  understand  speech  and  musical  tunes. 

4.  The  power  to  call  to  mind  objects  named. 

This  will  test  the  integrity  of  the  auditory-speeech  area  and 
of  the  association-tracts  between  other  sensory  areas  and  the 
temporal  convolutions. 

5.  The  power  to  understand  printed  or  written  words. 

6.  The  power  to  read  aloud  and  to  understand  wdiat  is  read. 

7.  The  power  to  recall  objects  whose  names  are  seen. 

8.  The  power  to  write  spontaneously,  and  to  write  the  names 
of  objects  seen,  heard,  etc. 

9.  The  power  to  copy  and  to  write  at  dictation. 

10.  The  power  to  read  understandingly  what  has  been 
written. 

These  tests  will  determine  the  condition  of  the  visual  word- 
memories  in  the  angular  gyrus,  and  of  the  connections  between 
this  area  and  surrounding  sensory  and  motor  areas. 

11.  The  power  to  speak  voluntarily,  and  if  it  is  lost,  the  char- 
acter of  its  defects. 

12.  The  power  of  repeating  words  after  another. 

This  will  test  the  mtegrity  of  Broca's  centre  and  its  associa- 
tion-tracts. 

I.  Word-Dcafiicss. — If  the  memory  of  the  sound  of  the  word 
is  lost,  the  word  cannot  be  called  to  mind  and  cannot  be  recognized 
when  heard.    Show  the  patient  a  watch,  and  he  is  unable  to  name 


60  DISEASES    OF   THE    NERVOUS    SYSTEM. 

it ;  tell  him  it  is  a  stone,  a  match,  a  watch,  and  notice  whether  he 
dissents  from  the  former  and  gives  signs  of  satisfaction  at  the 
last.  If  he  does,  he  has  only  auditory  amnesia,  but  not  word- 
deafness.  If  not,  he  is  word-deaf,  and  is  unable  to  understand 
what  is  said  to  him.  The  lesion  lies  in  the  posterior  half  of  the 
first  and  second  temporal  convolution  in  the  left  hemisphere  in 
right-handed,  in  the  right,  in  left-handed  persons.  This  is  one 
variety  of  aphasia  whose  lesion  is  well  known,  though  it  rarely 
occurs  alone. 

2.  W ord-Blindncss. — If  the  memory  of  the  appearance  of 
the  word  is  lost,  the  visual  image  of  it  cannot  be  called  to  mind 
or  recognized,  and  then  the  patient  will  be  unable  to  write  spon- 
taneously, for  he  cannot  remember  how  the  letter  looks  which  he 
wishes  to  write  ;  and  he  will  be  unable  to  read,  because  the  shapes 
of  the  letters  and  words  seen  arouse  no  recollection.  As  a  matter 
of  fact,  words  are  forgotten  more  easily  than  letters,  and  if  a 
patient  is  to  relearn  to  read  he  must  begin  with  letters  and  go  on 
to  words.  Figures  are  sometimes  recalled  when  words  are  for- 
gotten, and  many  a  patient  can  do  mathematical  calculations  on 
paper  who  cannot  read  or  write  ordinary  words.  The  reverse 
may  also  be  true,  the  patient  being  able  to  read  and  write,  but 
being  unable  to  understand  figures  or  calculate.  Such  patients 
may  also  play  cards  or  other  games,  if  they  are  not  physically 
blind.  It  is  not  infrequently  the  case  that  persons  who  are  thus 
word-blind  can  write  at  dictation,  or  copy,  and  yet  show  no  evi- 
dence of  understanding  what  has  just  been  read  or  written.  A 
distinction  must  be  made  between  those  who  can  and  cannot  do 
these  things,  though  its  pathological  basis  is  still  obscure.  The 
condition  of  visual  amnesia  with  word-blindness  is  due  to  a  lesion 

•  involving  the  inferior  parietal  convolutions  and  angular  gyrus, 
and  is  often  associated  with  psychical  blindness,  but  may  occur 
independently  of  it.  Word-deafness  and  word-blindness  fre- 
cjuently  occur  together,  and  then  the  lesion  is  found  involving 
both  the  temporal  and  the  angular  convolutions.  Some  cases  of 
this  condition  have  depended  on  a  deep  lesion  in  the  temporc- 
occipital  region,  breaking  the  association-tracts. 

3.  Motor  Aphasia. — If  the  memory  of  the  effort  needed  to 


/L>Wvji,-C<_<3 


J  -    iXirwhk     Bi^'V-rCu>i:tViAA 


-f.      ^6C,     ^AJL^^       ^tC^^t^^WV,     ^        ^^e^-<xA^ 


DISEASES    OF    THE    NERVOUS    SYSTEiM.  61 

pronounce  a  word  is  lost,  a  true  paralysis  of  active  speech  occurs, 
though  the  muscles  may  not  he  weakened.  This  is  the  ordinary 
form  of  motor  aphasia,  due  to  a  lesion  of  Broca^s^entre.  It  is 
to  be  noted  that  such  a  loss  of  speech  involves  a  loss  of  the  power 
of  repeating  words  after  another,  as  well  as  of  voluntary  speech, 
and  is  not  accompanied  by  any  inability  to  understand  spoken  or 
written  language.  In  the  uneducated,  as  in  children,  the  acts  of 
talking  and  writing  are  closely  joined,  as  may  be  seen  by  watch- 
ing the  lips,  which  move  in  the  act  of  writing.  But  among  those 
accustomed  to  write  much  these  acts  are  independent,  and  it  is 
probable  that  many  educated  aphasics  may  be  able  to  answer  ques- 
tions in  writing  when  their  efforts  at  speech  fail.  Reading  aloud 
will  also  be  lost  in  motor  aphasia,  for  here,  too,  the  inability  to 
articulate  hampers  the  patient. 

4.  Agraphia. — The  independence  of  the  effort-memory  neces- 
sary for  writing,  and  connected  with  movements  of  the  hand  from 
the  effort-memories  of  speech,  has  been  alluded  to.  When  these 
are  lost  alone  the  condition  is  known  as  agraphia.  In  such  a 
state  the  pen  cannot  be  used.  Copying,  writing  at  dictation,  and 
voluntary  writing  are  all  lost.  It  has  been  noted  already  that 
when  a  word  cannot  be  called  to  mind,  it  of  course  cannot  be  writ- 
ten. But  words  can  often  then  be  written  at  dictation,  if  the  per- 
son is  one  who  writes  much.  Hence  sensory  agraphia  and  motor 
agraphia  must  be  distinguished ;  the  former  being  a  part  of  word- 
blindness,  the  latter  not  at  all  associated  with  inability  to  read. 
The  lesion  of  motor  agraphia  is  unsettled,  though  a  few  facts  point 
to  the  posterior  part  of  the  second  frontal  convolution  as  the 
probable  seat  of  this  function.  It  is  not  unlikely,  however,  that 
the  more  exact  localization  of  fine  movements  of  the  thumb  and 
fingers  in  the  posterior  central  convolution  by  Horsley  may  be 
followed  by  the  discovery  of  the  writing  centre  in  this  vicinity. 

5.  Paraphasia. — These  forms  of  aphasia  are  due  to  a  loss  of 
distinct  memory-pictures.  The  several  memory-pictures  which 
are  united  in  the  word-image  may  thus  be  reasonably  regarded  as 
separate  from  one  another  in  their  location  in  the  brain.  But 
since  they  are  joined  together  to  form  the  word-image,  it  follows 
that  the  association-fibres  joining  the  various  areas  are  as  neces- 
sary to  the  use  of  even  a  single  word  as  the  various  areas  with 


62 


DISEASES    OF   THE   NERVOUS    SYSTEM. 


Fig.  17.- — The  Association  Fibres  in  the  Centrum  Ovale.  A,  Between  adjacent  con- 
volutions; B,  between  frontal  and  occipital  lobes;  C,  between  frontal  and  temporal 
lobes,  the  cingulum;  D,  between  temporal  and  frontal  lobes — lesion  of  this  tract 
causes  paraphasia;  E,  between  occipital  and  temporal  lobes — lesion  of  this  tract 
causes   word-blindness;     C.N.,   caudate  nucleus;     O.T.,   optic  thalamus. 

their  memories.  It  is  really  by  association  only  that  an  object  or 
a  word  becomes  a  subject  of  thought  or  use.  If  these  associations 
are  broken,  the  result  is  a  defect  of  language  characterized  by 
the  misplacement  of  words,  and  the  patient  talks  jargon. 

•There  are  many  forms  of  paraphasia  as  there  are  many  asso- 
ciation-tracts, and  it  is  not  yet  possible  to  assign  different  cases  to 
their  lesions. 

It  is  evident  that  many  differently  located  lesions  will  pro- 
duce disturbances  of  speech.  When  the  entire  cortex  is  diseased 
— as  in  paresis — aphasia  also  appears. 

Defects  in  the  appreciation  and  use  of  music  are  called  amu-. 
sia,  and  present  the  same  varieties  as  aphasia. 


The  Frontal  Region. 

There  appears  to  be  a  certain  relation  between  the  frontal 
lobes  of  the  brain  and  the  higher  forms  of  intellectual  activity, 
the  powers  of  fixing  the  attention  and  of  reasoning  and  of  self- 
control.  But  disease  here  does  not  cause  a  loss  of  any  one  mental 
faculty,  and  for  the  higher  powers  of  the  mind  a  general  integrity 


(f   ir*nr~c^    •^  <2_-t.-T^ 


1 


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6...    /kM^     oue^   ^^^t^^    -1^   L.^^^Y^JL^-.^^^^:fl:^^    '^-^^ 


DISEASES    OF    THE    NERVOUS    SYSTEM.  63.: 

of  the  entire  brain,  not  of  any  one  part,  is  necessary.  When  it  is 
considered  that  every  concept  is  made  up  of  numerous  memory- 
pictures  joined  together,  each  of  which  has  a  separate  location  in 
the  brain  cortex,  it  becomes  evident  that  to  the  process  of  thought 
a  healthy  state  of  the  entire  cortex  is  necessary,  and  also  of  the 
white  matter  beneath  it,  through  which  the  associating  fibres  pass. 
And  it  'is  therefore  impossible  for  a  single  lesion  anywhere  to- 
cause  a  loss  of  memory  or  of  imagination  or  of  judgment.  Yet 
for  the  co-ordination  of  facts  into  orderly  series,  for  comparison, 
and  for  analysis  of  knowledge  gained  through  the  senses,  the 
healthy  state  of  the  fontal  lobes  appears  to  be  necessary.  And 
lesions  in  the  frontal  region,  especially  upon  the  left  side,  are  quite 
uniformly  attended  by  mental  dulness,  apathy,  lack  of  power  of" 
concentration,  and  imperfect  self-control. 

There  are  large  areas  of  the  cortex  of  the  brain  whose  func- 
tion is  undetermined.  These  are  much  more  extensive  on  the- 
right  hemisphere  than  on  the  left.  There  are  no  definite  symptoms 
produced,  so  far  as  we  now  know,  by  lesions  in  these  areas ;  but 
the  negative  fact  is  certain,  that  lesions  in  them  do  not  cause  dis- 
turbances of  motion,  of  sensation,  or  of  speech. 

The  cortex  of  the  hemispheres  upon  the  base  of  the  brain 
lying  on  the  orbital  plate,  on  the  sphenoid  and  temporal  bones, 
and  on  the  tentorium  cerebelli,  has  as  yet  no  assignable  functions, 
and  lesions  in  these  regions  do  not  produce  recognizable - 
symptoms. 

Symptoms  of  Cortical  Disease. 

In  the  study  of  cases  of  cortical  disease,  it  is  necessary  at 
the  outset  to  distinguish  general  from  local  symptoms,  for  it  is 
the  latter  only  which  enable  one  to  locate  the  lesion.  General' 
Symptoms  are  those  which  are  common  to  various  kinds  of  brain 
disease  in  whatever  region  they  are  located.  They  are  headache, 
vertigo,  digestive  disturbances,  general  convulsions,  optic  neuritis, 
with  or  without  blindness,  delirium,  and  coma.  These  are  due- 
either  to  an  increase  of  the  intracranial  contents  (as  by  the  growth 
of  a  tumor)  and  consequent  presssure,  or  to  some  other  interfer- 
ence with  the  normal  condition  in  the  brain.     They  give  no  evi- 


64  DISEASES    OF    THE    NERVOUS    SYSTEM. 

dence  as  to  the  exact  region  of  the  brain  which  is  affected.    They 
merely  indicate  that  the  brain  is  diseased. 

Local  Symptoms,  on  the  other  hand,  depend  entirely  for  their 
production  upon  the  region  of  the  cortex  which  is  invaded.  They 
are  disturbances  of  motion  and  of  sensation  of  various  kinds,  and 
of  sensory  perception ;  disturbances  of  memory ;  and  loss  of 
speech.  They  may  be  divided  into  symptoms  of  irritation  and 
symptoms  of  destruction ;  and  it  is  not  infrequently  the  case  that 
the  former  precede  the  latter  in  the  course  of  a  disease.  An  irri- 
tative lesion  produces  symptoms  due  to  an  increased  activity  of 
the  area  affected ;  c.  g.,  spasms,  pain,  tingling  and  numbness, 
flashes  of  light,  sounds,  or  hallucinations  of  smell  and  taste.  A 
destructive  lesion  produces  symptoms  due  to  a  loss  of  function  in 
the  area  involved ;  e.  g.,  paralysis,  anaesthesia,  blindness,  deafness, 
loss  of  smell  and  taste,  and  of  the  use  of  language.  Each  of  these 
points  to  a  different  location  of  the  disease,  and  is  essential  to  its 
localization. 

II.  Tracts  Within  the  Brain. 
The  Association-Tracts. 

The  first  system  of  fibres  in  the  centrum  ovale  is  the  associa- 
tion system.     (See  Fig.  17.) 

It  can  be  shown  by  careful  dissection  that  each  convolution 
is  joined  to  the  two  adjacent  convolutions  by  fibres  which  pass 
around  the  separating  fissures.  Also,  that  bundles  of  fibres  exist 
which  pass  from  each  convolution  to  the  convolution  next  but  one, 
and  so  on.  Hence,  it  may  be  stated  that  each  convolution  has  a 
possible  connection  with  every  other.  Besides  this  association  of 
convolutions  by  small  bundles  of  fibres,  it  is  possible  to  find  a 
distinct  set  of  association-tracts  which  pass  between  more  or  less 
distant  regions.  One  such  tract  passes  from  the  frontal  lobe,  col- 
lecting its  bundles  from  all  three  convolutions,  backward  to  the 
occipital  lobe.  Another  tract  joins  the  occipital  with  the  anterior 
part  of  the  temporal  lobe.  Another  passes  from  the  upper  two 
temporal  convolutions  forward  to  the  third  frontal  convolution, 
passing  beneath  the  island  of  Reil.  And  a  tract  from  the  frontal 
to  the  posterior  temporal  area  may  also  be  found. 


DISEASES    OF    THE    NERVOUS    SYSTEM.  65 

The  function  of  these  association-fibres  is  to  form  the  phys- 
ical basis  for  the  association  of  concrete  memories  and  of  psychi- 
cal acts,  and  their  integrity  is  necessary  to  thought.  By  studying 
subjectively  the  association  of  ideas  in  the  mind  the  importance 
of  their  function  is  evident.  \Mien  they  are  destroved  bv  disease 
various  forms  of  paraphasia  appear. 

The  Commissural  Tracts. 

The  second  system  of  fibres  in  the  centrum  ovale  is  the  com- 
missural system.  This  joins  corresponding  areas  of  the  two  hemi- 
spheres with  one  another.  The  commissural  fibres  between  .the 
frontal,  parietal,  and  occipital  lobes  of  the  two  sides  pass  in  the 
corpus  callosum.  Those  from  the  temporal  lobes  pass  in  the  an- 
terior commissure.  The  function  of  these  fibres  is  to  harmonize 
the  action  of  the  two  hemispheres.  Simultaneous  movements  of 
like  nature  can  be  made  wath  great  facility  with  both  upper  ex- 
tremities. Movements  which  are  difficult  when  attempted  with 
the  left  hand  alone  become  easy  when  associated  with  correspond- 
ing movements  of  the  right  hand — as.  for  example,  drawing  a 
circle,  writing  one's  name.  It  is  the  commissural  fibres  joining 
the  motor  convolutions  only  which  can  be  thus  tested.  Failure 
to  perform  easily  corresponding  bilateral  motions  in  face,  hands, 
or  feet  would  indicate  some  obstruction  to  conduction  in  them. 


The  Projectiox-Fibres. 

The  projection  system  includes  those  fibres  which  join  a 
definite  area  of  the  cortex  with  parts  of  the  nervous  system  lying 
below  it,  viz.,  some  nervous  mechanism  in  the  basal  ganglia,  brain 
axis,  or  spinal  cord.  Indirectly,  through  the  medium  of  such 
mechanisms,  the  external  w^orld  is  projected  upon  the  brain  and 
reaches  consciousness,  and  voluntary  impulses  originating  in  the 
brain  are  sent  to  the  muscles.  The  fibres  gather  together  within 
the  hemisphere  at  the  upper  level  of  the  basal  ganglia,  and  either 
end  in  the  optic  thalamus  or  go  on  between  these  ganglia  through 
the  internal  capsule  to  the  brain  axis  and  spinal  cord. 

The  majority  of  these  fibres  end  in  the  optic  thalamus,  which 


66  DISEASES    OF    THE    NERVOUS    SYSTEM. 


Fig.  i8. — The  Projection  Tracts  Joining  the  Cortex  with  Lower  Nerve  Centres. 
Sagittal  section  showing  the  arrangement  of  tracts  in  the  internal  capsule.  A, 
Tract  from  the  frontal  lobe  to  the  pons,  thence  to  the  cerebellar  hemisphere  of  the 
opposite  side;  B,  motor  tract  from  the  central  convolutions  to  the  facial  nucleus  in 
the  pons  and  to  the  spinal  cord;  its  decussation  is  indicated  at  K;  C,  sensory  tract 
from  posterior  columns  of  the  cord,  through  the  posterior  part  of  the  medulla,  pons, 
crus,  and  capsule  to  the  parietal  lobe;  D,  visual  tract  from  the  optic  thalamus  (O.T.) 
to  the  occipital  lobe;  E,  auditory  tract  from  the  internal  geniculate  body  (to  which 
a  tract  passes  from  the  VIII.  nerve  nucleus  [J]  to  the  temporal  lobe;  F,  superior 
cerebellar  peduncle;  G,  middle  cerebellar  peduncle;  H,  inferior  cerebellar  peduncle; 
CN,  caudate  nucleus;  C.Q.,  corpora  quadrigemina;  \'t.,  fourth  ventricle.  The 
numerals  refer  to  the  cranial  nerves. 

is  thus  connected  with  all  parts  of  the  cortex  of  the  brain.  Of 
the  function  of  these  we  know  very  little.  Two  large  bundles, 
however,  are  separable  from  the  mass. 

The  Visual  Tract. — One  of  these  passes  inward  and  forward 
from  the  occipital  lobe,  and  joins  the  pulvinar  of  the  thalamus 
and  the  external  geniculate  bodv.    This  is  the  visual  tract.     (Fig. 

14.) 

The  optic  nerves  decussate  partially  at  the  chiasm,  so  that 


DISEASES    OF    THE    NERVOUS    SYSTEM.  67 

each  optic  tract  contains  fibres  from'both  rctinse.  Each  tract  passes 
to  the  optic  thalamus,  external  geniculate-  body,  and  anterior  cor- 
pus quadrigeminum.  Thence  the  fibres  of  the  visual  tract  pass 
out,  to  turn  backward  through  the  internal  capsule  and  through 
the  centrum  ovale  to  the  cortex  of  the  occipital  lobe.  A  lesion 
anywhere  in  this  course  causes  homonymous  hemianopsia. 

The  Auditory  Tract. — A  second  bundle  passes  from  the 
temporal  lobe  upward  to  the  thalamus,  internal  geniculate  body, 
and  posterior  corpus  quadrigeminum,  in  which  the  auditory  tract 
from  the  acoustic  nucleus  ends.  This  conveys  impulses  of  sound 
from  both  ears  to  each  temporal  lobe,  and  is  the  auditory  tract. 
These  are  the  only  bundles  of  the  thalamic  radiations  whose  func- 
tion is  determined.     (Fig.  i8E.) 

Some  of  the  projection-fibres  pass  on  through  the  internal  cap- 
sule without  communicating  with  the  basal  ganglia,  and  of  these 
we  know  three  distinct  bundles.     (Fig.  i8  A.) 

The  first  is  collected  from  the  three  convolutions  of  the  fron- 
tal lobe,  and  passing  between  the  caudate  and  lenticular  nuclei  in 
the  anterior  division  of  the  interal  capsule,  descends  in  it  to  the 
base  of  the  brain,  and  issuing  in  the  inner  third  of  the  foot  of  the 
crus  cerebri,  passes  down  to  the  pons,  where  it  terminates  in  nu- 
clei lying  in  the  ventral  half.  The  nuclei  thus  reached  by  these 
fibres  are  also  joined  by  other  fibres  from  both  hemispheres  of  the 
cerebellum,  which  enter  the  pons  at  its  lateral  surfaces  in  the  mid- 
dle peduncles.  Thus  it  is  evident  that  a  connection  exists  between 
each  frontal  lobe  and  both  cerebellar  hemispheres,  the  crossed 
connection  being  greater  than  the  direct  one.  Of  the  function  of 
this  tract  we  know  nothing. 

The  Motor  Tract. — The  second  bundle  of  the  projection  sys- 
tem is  the  luotor  tract.  It  comes  from  the  posterior  part  of  the 
third  frontal  convolution,  the  two  central  convolutions,  and  from 
the  paracentral  lobule,  and  passes  out  of  the  base  through  the 
middle  third  of  the  crus  cerebri.  Its  fibres  collect  at  the  middle 
portion  of  the  upper  surface  of  the  internal  capsule,  those  from 
the  lower  parts  of  the  cortex  passing  straight  inward,  those  from 
the  upper  parts  curving  outward  and  downward  to  pass  around 
the  side  of  the  lateral  ventricle.     Thus  within  the  centrum  ovale, 


DISEASES    OF    THE    NERVOUS    SYSTEM. 


Fig.  19. — The  Motor  Tract.  S,  Fissure  of  Sylvius;  N.L.,  lenticular  nucleus;  O.T., 
optic  thalamus;  N.C.,  caudate  nucleus;  C,  crus;  P,  pons;  M,  medulla;  O,  olivary 
body.  The  tracts  for  face,  arm,  and  leg  gather  in  the  capsule  and  pass  together  to 
the  lower  pons,  where  the  face  fibres  cross  to  the  opposite  \'II.  nerve  nucleus, 
while  the  others  pass  on  to  the  lower  medulla  where  they  partially  decussate,  to 
enter  the  lateral  columns  of  the  cord;  the  non-decussating  fibres  pass  to  the  an- 
terior median  columns.  The  effect  of  a  lesion  situated  at  three  points  in  the  tract 
is  shown  on  the  left  side   of  the  figure. 

these  fibres,  if  looked  at  from  in  front,  appear  like  the  sticks  of 
a  fan,  and  like  those  sticks  their  relative  position  is  altered  in  the 
point  of  junction,  where  those  passing  inward  from  the  lowest 
part  of  the  cortex  lie  in  front  of  those  which  pass  downward 
from  its  upper  part.  Thus  in  the  capsule  the  order  from  before 
backward  is,  iirst,  the  fibres  conveying  speech  impulses  to  the 
pons  and  medulla ;  second,  the  fibres  conveying  facial-motor  im- 
pulses to  the  pons;  third,  the  fibres  destined  to  the  arm  centres  of 
the  cord ;  fourth,  the  fibres  transmitting  impulses  to  the  leg 
centres  in  the  cord.  The  fibres  conveying  impulses  to  the  muscles 
of  the  trunk  lie  between  those  to  the  arm  and  leg.     (See  Fig.  20.) 


DISEASES    OF    THE    NERVOUS    SYSrE>r.  69 

From  the  anterior  half  of  the  posterior  division  of  the  capsule 
this  tract  passes  through  the  mi<ldlc  third  of  each  crus,  through 
the  pons  (where  the  division  to  the  facial  nucleus  crosses  to  the 
opposite  side  and  ends),  and  thence  by  way  of  the  pyramids  of  the 
medulla  to  the  crossed  pyramidal  and  direct  anterior  median  col- 
umns of  the  spinal  cord.  It  is  evident,  however,  that  the  con- 
centration of  this  tract  is  much  greater  in  the  capsule  than  in  the 
centrum  ovale,  where  the  individual  fibres  are  scattered  among 
the  other  systems  and  occupy  but  a  small  area  from  before  back- 
ward. 

Lesions  beneath  the  third  frontal  convolution  of  the  left  side 
produce  motor  aphasia.  Lesions  beneath  the  central  convolutions 
in  the  centrum  ovale  produce  paralysis,  which  will  vary  according 
to  the  position  of  the  lesion.  The  nearer  the  lesion  lies  to  the  cor- 
tex the  more  will  the  symptoms  resemble  those  of  cortical  disease, 
monoplegia  being  the  rule.  The  nearer  the  lesion  to  the  point  of 
junction  at  the  capsule  the  more  will  the  symptoms  resemble  those 
of  capsule  lesion,  hemiplegia  being  the  rule.  When  the  motor 
tract  is  injured  bv  a  lesion  in  the  lower  half  of  the  pons,  the  result 
is  paralysis  of  the  face  on  the  side  of  the  lesion  and  of  the  arm 
and  leg  on  the  opposite  side  (alternating  paralysis). 

TJic  Sensory  Tracts. — The  third  set  of  fibres  of  the  projec- 
tion system  include  those  which  lie  just  posterior  to  the  motor 
tract,  and  which  pass  inward  from  the  parietal  convolutions. 
These  take  a  similar  course  to  those  of  the  motor  tract,  and  fill 
up  to  a  considerable  extent  the  space  between  it  and  the  radiation 
of  the  visual  tract,  toward  the  occipital  lobe.  The}'  are  mingled 
with  fibres  which  pass  to  the  optic  thalamus,  but  are  separable  from 
them  in  foetal  brains,  and  may  be  traced  down  through  the  capsule 
to  the  tegmentum  of  the  crus,  where  they  divide  into  a  portion 
going  to  the  lemniscus,  and  a  portion  going  to  the  formatio  reticu- 
laris. The  fibres  can  be  traced  through  these  tracts  dowaiward  to 
the  medulla  and  through  the  sensory  decussation  to  the  posterior 
pyramids  of  the  medulla  in  w'hich  the  posterior  columns  of  the 
spinal  cord  begin.  See  Figs.  21-24.)  This  set  of  fibres  conveys 
the  sensations  of  touch,  pain,  temperature,  and  muscular  sense, 
and  lesions  in  its  course  will  cause  disturbance  of  these  sensations. 


70 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


Fig.  20. — Horizontal  Section  through 
the  Brain.  (After  Strumpell.)  NC, 
nucleus  caudatus;  F,  fornix;  IC, 
anterior  half  of  internal  capsule;  OT , 
optic  thalamus;  Fa,  facial  tract;  M, 
motor  tract;  S,  sensory  tract;  O, 
visual  tract,  in  posterior  half  of  in- 
ternal capsule;  IR,  island  of  Reil; 
NL  nucleus  lenticularis;  EC,  ex- 
ternal capsule;  V,  lateral  ventricle, 
posterior  cornu. 

Lesions  of  the  corpora  quad 
ness,  and  ophthalmoplegia. 


Like  lesions  in  the  motor  tract, 
the  rule  obtains  that  the  nearer 
the  cortex  the  more  likely  is  the 
lesion  to  cause  an  affection  of  a 
single  limb,  while  the  nearer  the 
capsule  the  more  likely  is  the 
symptom  produced  to  be  liemi- 
ansesthesia.  A  lesion  in  the 
•lower  half  of  the  pons  may  pro- 
duce alternating  hemianaesthe- 
sia,  the  face  being  anaesthetic  on 
the  side  of  the  lesion,  nnd  the 
limbs  on  the  opposite  side. 

From  these  facts  it  is  evi- 
dent that  a  lesion  which  lies  in 
the  centrum  ovale,  at  any  point 
posterior  to  the  praecentral  fis- 
sure of  the  frontal  lobe,  may 
produce  recognizable  symp- 
toms, for  it  must  affect  either  the 
motor,  or  the  sensory,  or  the 
visual,  or  the  auditory  tracts,  or 
individual  fibres  of  those  tracts. 

■     in.  The  Basal  Ganglia. 

The  symptoms  produced  by 
lesions  in  the  basal  ganglia — 
corpora  striata  and  optic  thala- 
mus— are  not  to  be  distinguised 
from  those  caused  by  lesions  of 
the  projection-tracts  which  lie 
near  them  in  the  internal  capsule, 
rigemina  cause  nystagmus,  blind- 


IV.  The  Cerebellum. 

The  cerebellum  is  the  central  organ  of  equilibriuuL     It  is 
joined  to  the  spinal  cord  by  the  direct  cerebellar  column,  which 


TheMatarTmc/' 


aieral pyramuLii 
tract 


r^ 


Fiucajrt&f^uus 


•sterOT-TTL  body 


fuuc^racvles 

71UC  curteai:-: 

■Xateml  coliurtr. 


•  (^n,  i/t£  firr-rf 


Fl.;.    -IX 
The  Motor  Tract  in  the  Cerebral  Axis. 


Fig.  22 

The  Tract  of  the  Tactile  Sense. 


Cen-M'u.'n  > 


rcuc-Cunea/us 
Meckdia 


Memory 
decursatiJjn 


,Qii^ 


LunuLbSCUs 

Jted  rvurleur 


Cervbrt 


TAele. 


Fk;.   23 


Fk;.   24 


The  Tract  of  Muscular  Sense. 


DISEASES    OF    THE    NERVOUS    SYSTE^[.. 


carries  sensory  impulses  up  to  it  through  the  inferior  peduncle. 
It  is  joined  to  the  motor  tract  by  the  middle  peduncle,  which  con- 
veys impulses  to  the  pons  and  thence  to  the  spinal  cord,  directing 
balancing  motions.  It  is  joined  to  the  cerebral  hemispheres  both 
by  the  middle  and  superior  peduncles,  whose  exact  functiona  are 
unknown. 

Lesions  of  the  cerebellum,  or  of  its  peduncles,  cause  stagger- 
ing g'ait.  This  differs  from  that  in  locomotor  ataxia,  for  there  is 
no  ataxia  of  the  limbs  when  the  patient  lies  down,  giving  support 
to  the  body.  When  the  middle  peduncle  is  irritated  the  patient 
staggers  toward  the  lesion  ;  when  it  is  destroyed  he  staggers  away 
from  the  lesion.     Lesions  of  the  cerebellum  also  produce  vertigo. 

\'.  The  Cerebral  Axis. 

The  various  long  tracts  which  join  the  brain  to  the  spinal  cord 
pass  through  the  crus  cerebri,  pons,  and  medulla  near  to  the 
nuclei  of  origin  of  the  cranial  nerves.  These  tracts  are  shown  in 
Figs.  21-24.    The  cranial  nerve  nuclei  were  shown  in  Fig.  7. 

Lesions  of  the  cerebral   axis, 
^^1?>  such     as     small     hemorrhages, 

small  areas  of  softening,  or  tu- 
mors destroy  these  tracts  and 
also  these  nuclei.  The  tracts 
as  a  rule  decussate  on, entering 
the  cord,  hence  a  unilateral  le- 
sion of  the  cerebral  axis  causes 
motor  or  sensory  symptoms  in 
the  extremities  of  the  opposite 
side  The  nuclei  of  the  cranial 
nerves  send  those  nerves  directly 
outward  without  decussating; 
hence,  a  unilateral  lesion  of  the 
cerebral  axis  causes  motor  or 
sensory  symptoms   in    the    face 

Fic.  Jt. — The  Motor  Tract  in  Pons  and  ^i  •  i  -r*  .1 

Medulla.    Lesion  at  A  causes  hemi-    ou    the    Same    Side.      From    the 

plegia  of   side   opposite   to   lesion;     le-  f^nmhinpl-inrt     of     tViPQP     tivn    cf^tQ 

sion    at    B    causes    alternating    paraly-  COmOinatlOn     Ot     tnCSC     tU  O    SCt^ 

sis;     lesion    at    C   causes    paralysis    of  ^f  cvmnl-nTTT;  if   IQ    <^a>ivr    fo    rliacr 

tongue   on   side   of   lesion   and    of   ex-  *-"^  S}.  mpioms  11   IS    eas\     tO    Qiag- 

tremities   of   opposite   side;     lesion   at  rin<^ripatp    a     Ip^inn     of    tViP    rf^rp- 

D    causes    paralysis    of    extremities    of  "OStlCaie    d     ICblOn     Or     me    CerC- 

opposite    sides;      lesion    at    E    causes  'hral   nvit;  ^^pp   Fio-     •> ^  \ 

paralysis  of  extremities  of  both  sides.  ^^^^  '^■^'^-        V^^^  ^  ^&-    "^-Z 


"VE  NUCLEUS. 


yifnUOLEjs.O 


Wj^lERlT. 


THE  CEREBRAL  DISEASES  OF  THE  VASCULAR 

ORIGIN. 


Hemorrhage,  E:\ibolism,  Thrombosis,  "Apoplexy."    ■ 

The  most  common  cerebral  diseases  are  those  due  to  a  rup- 
ture of  a  vessel  in  the  brain,  cerebral  hemorrhage,  or  to  a  stoppage 
in  a  cerebral  vessel,  cerebral  ciiibolisiii  and  cerebral  tliroinbosis. 

The  cerebral  circulation.     See  "Quain's  Anatomy." 

Pathology. — The  condition  which  leads  to  such  diseases  is 
chronic  endarteritis :  a  chronic  inflammatory  process  in  the  intima 
and  muscular  coats  of  the  vessels  vith  a  production  of  new 
cellular  tissue  which  may  (i)  go  on  tmtil  it  obliterates  the 
lumen  of  the  vessel,  producing  thrombosis;  or  (2)  undergo  cal- 
careous degeneration,  roughening  the  wall  and  inducing  fibrin 
deposits,  which  may  occlude  the  vessel,  producing  thrombosis, 
or  be  washed  onward,  producing  embolism;  or  (3)  undergo  fatty 
degeneration,  thus  eroding  the  intima  and  weakening  the  muscu- 
lar coat,  causing  aneurisms  (miliary  or  larger)  which  rupture, 
producing  cerebral  hemorrhage.  See  Delafield  and  Prudden's 
"Pathology." 

Pathology  of  Cerebral  Hemorrhage.- — The  vessel  ruptures. 
The  blood  spreads  out  in  the  membranes,  filling  the  fissures  and 
depressing  the  cortex,  or  if  the  hemorrhage  is  subcortical,  tears 
the  surrounding  brain.  A  clot  forms,  thin  and  flat  on  the  cortex, 
globular  in  the  brain,  which  tears  and  compresses  the  brain- 
tissue  around  it.  This  clot  gradually  shrinks  and  undergoes  ab- 
sorption, leaving  a  hsematin  stain ;  the  disintegrated  brain-tissue 
undergoes  fatty  degeneration  and  absorption.  There  remains  a 
mass  of  softened  tissue  without  or  with  a  connective-tissue  wall, 
or  finally  a  cyst,  or  a  mass  of  sclerotic  tissue  or  merely  a  scar. 
The  torn  brain  never  reunites.  From  the  point  of  laceration 
degeneration  begins,  which  e.xtends  along  the  various  tracts,  e.  g.. 


ly^  f 


DISEASES    OF    THE    NERVOUS    SYSTEM.  75 

desccndins;-  (legcneratiun  in  niutor  tract  through  the  cerebral  axis 
and  spinal  cord,  or  ascending  degeneration  in  sensory  tracts  to  the 
cortex.  When  the  presstire  is  removed  the  cortex  may  resume  its 
function  or  the  uninjured  tracts  may  resume  their  functions. 
Hence  partial   recovery  is  the  rule  after  cerebral  hemorrhage. 

Pafholoi^x  of  Cerebral  Eiiibolisin  or  TJiroiiibosis. — The  vessel 
being  occluded,  the  brain-tissue  which  is  supplied  with  blood 
through  it  is  cut  oft"  from  its  nutrition.  The  first  arrest  of  blood 
supply  is  extensive,  but  when  collateral  circulation  is  established 
the  final  area  or  region  which  softens  may  be  small.  In  the  cortex, 
the  collateral  supply  by  anastomosing  vessels  is  extensive.  In  the 
basal  ganglia  and  capsule  it  is  very  imperfect.  Hence  the  perma- 
nent effect  of  occlusion  is  more  serious  in  the  arteries  entering  the 
base  than  in  the  small  branches  in  the  cortex.  If  large  vessels  in 
the  cortex,  e.  g.,  a  main  branch  of  a  Sylvian  artery,  is  plugged, 
the  area  of  softening  may  be  extensive.  A  fatty  degeneration  and 
a  necrosis  of  brain-tissue  follow  the  occlusion  of  the  vessel.  In 
the  softened  tissue  there  are  at  first  extravasations  of  venous  blood 
(red  softening)  ;  later  these  are  absorbed  and  the  tissue  in  a  stage 
of  fatty  degeneration  is  yellow  (yellow  softening).  If  there  is 
simple  necrosis  without  extravasation  or  fatty  degeneration,  the 
brain  has  its  natural  color  but  is  soft  (white  softening).  The 
softened  tissue  contracts,  leaving  a  depression,  or  a  cavity,  or  a 
scar  ;  in  some  cases  a  cyst  with  smooth  walls  and  serous  contents. 

The  Sifiiafion  of  the  Lesion. — Cerebral  hemorrhage :  in  basal 
ganglia  involving  the  internal  'capsule  in  fiftv  per  cent.,  next  in 
frequency  in  centrum  ovale,  cortex,  pons,  and  ventricles  ;  very 
rarely  in  cerebellum. 

Cerebral  embolism,  forty-nine  per  cent,  left ;  forty-one  per 
cent,  right ;  ten  per  cent,  both  hemispheres.  Central  ganglia  and 
capsule,  sixty  per  cent. ;  next  in  frequency  cortex  supplied  by 
middle  cerebral  artery,  (i)  motor  area,  (2)  aphasic  area,  (3) 
visual  area.  Least  frequent  pons  and  anterior  or  posterior  cere- 
bral arteries. 

Cerebral  thrombosis  is  middle  cerebral,  basilar,  vertebral,  and 
anterior  and  posterior  cerebral  vessels  in  order  of  frequency 
named. 

Etiology. — Thrombosis  is  common  below  age  of  forty-five ; 


76  DISEASES    OF    THE    NERVOUS    SYSTEM. 

hemorrliag"e  after  forty-five  ;  age  of  maximum  liability  to  hemor- 
rhage, fifty  to  sixty.  ]\Iales  more  liable  than  females  to  hemor- 
rhage. Predisposing  causes  of  endarteritis  are  gout,  lithaemia,. 
alcoholism,  and  syphilis  ;  associated  diseases  are  nephritis,  endo- 
carditis, and  emphysema.  Anything  which  increases  the  heart  £>  cL^^-l^  co- 
action  may  cause  cerebral  hemorrhage,  e.  g.,  fright,  anger,  exer- 
tion, cold  bath.  Anything  which  weakens  its  action  may  cause 
thrombosis.  o-<  ^^/^.r-cU^t^'^  ^^iU^^^Ly,    f^-<-^  • 

Syinptouis. — Preliminary :  For  months  before  the  onset,  ver- 
tigo, insomnia,  headache,  inattention,  and  imperfect  memory. 
Temporary  attacks  of  numbness  in  one-half  of  the  body. 

Sudden  onset,  "apoplexy,"  loss  of  consciousness.  The  result 
depends  on  the  size  and  rapidity  of  hemorrhage,  or  on  the  size  of 
the  vessel  occluded. 

Paralysis  of  one-half  of  the  body  (hemiplegia),  with  coma 
and  convulsions,  is  the  ordinary  form.  Face,  red  ;  pulse,  slow, 
high  tension,  full ;  respiration,  deep,  stertorous.  Temperature 
normal,  but  after  some  hours  high,  102"  to  104*^  F.  Deviation  of 
eves  and  head  may  occur  in  large  lesions  ;  the  patient  looks  toward 
the  side  of  lesionr  Pupils  vary.  Irlequality  is  most  important 
symptom,  usually  dilated  on  side  of  lesion.  Hemiplegia,  hemian- 
sesthesia,  and  hemianopsia,  at  first.  Reflexes  suspended  ;  inhib- 
ited by  irritation  for  a  short  time,  then  exaggerated  permanently.<rK/^^*^^<i 
Rigidity  of  limbs  when  hemorrhage  is  large  or  into  the  ventricle ; 
convulsion  when  hemorrhage  is  on  cortex  .or  in  ventricle.  Urine 
retained  ;  contains  albumen  and  sugar,  or  may  be  passed  involun- 
tarih".  \\-^ajujumJmx.  l>\ti.<jULL* —  -yu-a^  A^^^^SXc^  ^^    y-^i^ 

Death  may  occur  in  one  or  two. days,  in  coma,  with  tempera- 
ture of  108"  Y.  <J~^  '^  f^^    ^^  • 

Usually  there  is  a  slow  recovery  of  consciousness  and  perma- 
nent paralysis,  which  gradually  decreases  during  a  year,  and  then 
remams  stationary.  "  ' 

In  lighter  cases  there  may  be  no  loss  of  consciousness,  but 
partial  hemiplegia  or  arrest  of  any  cortical  function. 

The  permanent  symptoms  a  week  after  the  acute  onset  indi- 
qate  the  situation  of  the  lesion.  The  symptoms  which  remain  at 
the  end  of  a  month  indicate  its  extent ;  e.  g.,  hemiplegia  with  hemi- 


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DISEASES    OE    'rill-:    XERVOUS    SYSTEAL  m 

anaesthesia  and  hemianopsia  at  first:  and  permanent  paralysis, 
not  total,  in  arm  and  leg-  onl)-,  without  sensory  affection  finally. 
In  some  cases  there  is  a  development  after  two  months  of  con- 
tractures in  the  paralyzed  limhs.  This  indicates  the  existence  of 
descending  degeneration  in  the  motor  tract. 

Course. — After  the  acute  onset,  in  which  the  patient  is  con- 
fined to  bed  for  two  weeks  to  two  months,  depending  on  the 
severity,  the  improvement  begins ;  the  chief  symptom  being  hemi- 
plegia. The  face  is  flat  on  the  paralyzed  side,  and  is  slightly 
drawn  by  the  healthy  muscles  away  from  the  paralyzed  side  so 
that  the  mouth  is  crooked.  The  eye  can  be  closed  (vs.  facial 
palsy),  and  can  be  moved  (vs.  ophthalmoplegia).  The  tongue 
deviates  toward  the  paralyzed  side.  The  finer  motions  of  the 
hand  and  arm  are  more  permanently  affected  than  elbow  or  shoul- 
der motions ;  and  the  upper  extremity  is  carried  in  a  flexed  posi- 
tion. The  leg  is  stifif  and  extended,  does  not  bend  easily  at  the 
knee,  and  the  foot  is  dragged  on  its  inner  edge  and  swung  around 
in  walking.  The  muscles  of  the  trunk  and  respiration  are  very 
rarely  affected.  The  bladder  and  rectum  may  not  be  under  full 
control.  There  may  be  a  diminution  of  sensation  in  the  paralyzed 
side,  and  possibly  hemianopsia.  Hemianaesthesia  or  hemianopsia 
may.  remain  without  hemiplegia.  A  total  loss  of  all  senses,  smell, 
taste,  sight,  hearing,  and  touch  on  one  side  only,  occurs  in  hysteria 
only.  The  tendon  reflexes  are  usually  much  increased  on  the  par- 
alyzed side,  and  are  somewhat  increased  on  the  other  side  as  well. 
The  contractures  which  develop  may  cause  pain,  because  the 
limbs  are  rigid.     Otherwise  there  is  no  pain. 

Aphasia  of  some  kind  often  accompanies  right  hemiplegia, 
or  may  occur  alone.     (See  page  56.) 

Some  mental  symptoms  are  usually  observed  after  an  apo- 
plexy, and  ma}'  be  the  only  permanent  symptoms.  There  may  be 
a  lack  of  control  of  the  emotions,  so  that  the  patient  laughs  or 
cries  with  little  cause;  an  irritability  of  temper;  a  lack  of  judg- 
ment ;  imperfect  memory  of  recent  events ;  imperfect  power  of 
concentrated  attention ;  general  bewilderment,  so  that  the  patient 
does  not  recognize  his  surroundings  or  friends ;  mild  delirium  or 
delusions ;  or  even  dementia.  These  usually  pass  away  gradually, 
but  sometimes  remain. 


78  DISEASES    OF   THE    NERVOUS    SYSTEM. 

The  various  symptoms,  motor,  sensory,  aphasic,  or  mental,, 
depend  on  the  situation  of  the  lesion,  and  enable  a  conclusion  to 
be  arrived  at  regarding  it. 

In  any  case  epileptiform  attacks  may  develop,  and  continue 
at  long  intervals  after  an  apoplexy. 

Diagnosis.  Cerebral  HeinonduLS'^. — In  old  persons  with 
atheromatous  arteries  and  hypertrophied  heart.  Sudden  onset  of 
coma  during  exertion  or  in  excitement.  Coma  deepens ;  tempera- 
ture falls  to  97°  to  95''  F.  in  an  hour;  after  three  hours  rises  to 
101°  F.  Gradual  recovery  of  consciousness  in  three  to  five  days, 
with  permanent  symptoms  of  hemiplegia. 

Cerebral  Embolism. — At  any  age  with  heart  disease,  or  after 
childbirth.  Sudden  onset  with  no  loss  of  consciousness  or  slight 
condition  of  mental  confusion,  or  rapid  return  of  consciousness. 
Temperature  does  not  fall,  but  may  rise  to  102°  F.  Improve- 
ment occurs  within  twenty-four  hours  to  a  marked  degree,  but 
symptoms  return  in  three  or  four  days  and  are  permanent,  either 
monoplegia,  or  hemiplegia,  or  aphasia.  Jacksonian  epilepsy  may 
develop  after  a  few  months. 

Cerebral  Thrombosis. — At  any  age,  but  chiefly  in  syphilitic 
persons  and  in  rnict^-'aged  men.  Premonitions  usually  occur. 
Slower  onset  without  coma,  but  dulness  of  mind.  Consciousness 
returns  soon,  if  lost.  Temperature  does  not  fall ;  may  rise  to 
100"  F.     The  paralysis  resembles  that  in  embolism. 

The  diagnosis  between  these  three  conditions  is  never  posi- 
tive. /XM^ttrVjAlc^  0^   fi^.  h\yrh<.   (LLa-^iTiM^   i^iyc/u.^  u^     L  TLc  ta^^JL^ 

Causes  of  coma  other  than  apoplexy :  Syncope,  epilepsy,, 
uraemia,  diabetes,  alcoholism,  opium  poisoning,  sunstroke,  cerebral 
injury.  Apopletic  coma  is  deep  and  patient  cannot  be  aroused. 
Face  is  congested,  eyes  turned  to  one  side,  pupils  unequal,  pa- 
ralysis is  unilateral,  limbs  may  be  rigid ;  appearance  indicates  pre- 
vious convulsions.  Physical  examination  reveals  absence  of  in- 
jury and  presence  of  predisposing  disease,  e.  g.,  atheroma,  en- 
darteritis, cardiac  disease,  albuminuria,  syphilitic  scars.  The 
absence  of  diagnostic  signs  of  other  causes  of  coma  confirms  the 
diagnosis  of  apoplexy.  Reflex  movements  can  be  caused  on  non- 
paralyzed  side  by  producing  pain.     The  tendon  reflexes  are  often 


t:«-ex-     ,/w. 


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hMjlJnJljU' 


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{YZ^J-X^^^,^  .  JQ^^^^^L^^    ^=^-x.uu[-^  M^cjz>^.j^      U^       '^      .w^ 

(f-^^tA. a,<;2.-cjH.vtA     lA_<to     <*M^uo-^\x.<..^.y\'2-^     fyA^^j-t.^    c^)-^..t-^     uiju^^j^  &ijHAjrJ^-ii.  ' 

I.,    ,      lAO  I     n  „    ts  ^  'j 


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DISEASES    OE    THE    NERVOUS    SYSTEM.  79 

lost  at  the  onset.     The  eremasteric  rellex  is  always  lost  on  the 
paralyzed  side. 

Prognosis  depends  on  the  depth  of  coma,  on  the  condition  of 
pulse  and  respiration,  on  the  constitution  and  age  of  the  patient, 
and  on  the  number  of  previous  attacks. 

Treatment    in    stage   of   apoplexy :   Rest ;   quiet ;   ice-bag   to 
head ;  venesection  in  plethoric  cases ;  purgatives  of  a  drastic  na-  (>iJt^ 
ture ;  stimulants  if  heart  failure  is  present. 

P\ir  hemiplegia  :  Exercise  ;  massage  ;  faradism  to  the  mus- 
cles for  purpose  of  exercise. 

^Medicines  are  of  no  use  in  either  stage. 

Cerebral  Atrophy. 

Cases  of  cerebral  disease  in  children,  either  unilateral  or  bi- 
lateral, present  some  peculiar  features  of  three  different  types. 

First,  cases  of  hemiplegia  with  or  without  athetosis. 

Secondly,  cases  of  mental  defects  of  various  grades. 

Thirdly,  cases  of  sensory  defect  of  different  types.  Epilepti- 
form seizures  of  petit  inal  or  of  grand  iiial  type  occur  frequently 
in  patients  who  may  be  assigned  to  any  one  of  these  groups. 

I.  Infantile  HciniplcQia. — The  symptoms  are  the  sudden  de- 
velopment of  a  unilateral  paralysis  after  a  series  of  convulsions 
attended  by  high  fever  and  its  attendant  discomforts,  and  a  period 
of  unconsciousness  of  varying  duration ;  then  a  gradual  improve- 
ment in  the  paralysis  after  the  active  manifestations  of  the  onset 
have  subsided  ;  and  finally,  a  stationary  condition,  in  which  the 
face  is  but  slightly  affected  in  its  voluntary  or  automatic  move- 
ments ;  the  speech  is  usually  regained,  if  it  had  been  lost;  the  arm 
is  quite  seriously  paralyzed,  the  fingers  being  stiff  and  awkward, 
and  sometimes  being  in  constant  slow  involuntary  motion  (athe- 
tosis) ;  the  leg  is  held  rather  rigid,  so  that  the  child  limps  in 
walking,  and  often  develops  a  club-foot.  There  are,  of  course, 
on  the  one  hand,  light  cases  in  which  the  symptoms  finally  amount 
merely  to  clumsiness  in  the  fingers.  There  are,  on  the  other  hand, 
severe  cases  in  which  a  double  hemiplegia  has  occurred,  both 
halves  of  the  body  being  equally  affected,  and  in  which  both  arms 
are  useless  and  both   legs  so  stiff,   so  closely  adducted,   and  so 


so  DISEASES    OF   THE    NERVOUS    SYSTEM. 

helpless,  that  walking  is  impossible  (diplegia).  The  latter  are 
cases  in  which  all  the  symptoms  date  from  birth.  In  all  cases 
the  paralyzed  limbs  are  found  to  be  affected  in  their  growth  and 
development,  so  that  they  are  smaller,  colder,  stiffer,  and  weaker 
than  the  others ;  the  reflexes  are  exaggerated,  but  the  electrical 
reactions  are  not  qualitatively  changed,  and  the  sensation  is 
normal.  This  condition  remains  through  life  as  a  permanent 
defect,  and  although  the  division  of  contractured  muscles  or  ten- 
dons and  the  application  of  ingenious  apparatus  may  correct  de- 
formities and  make  the  paralyzed  parts  fairly  useful,  and  although 
the  application  of  electricity  to  the  muscles  chiefly  affected  may 
increase  their  nutrition  and  this  prevent  contracture  which  comes 
from  the  unbalanced  strain  between  the  various  muscles,  yet  any 
great  degree  of  improvement  is  impossible.  In  more  than  one- 
half  of  these  cases  epileptic  attacks  are  of  frequent  occurrence. 

The  cases  which  date  from  birth  must  be  divided  into  those 
in  which  there  has  been  evidence  of  traumatism  during  labor, 
and  those  in  which  there  was  none.  In  the  former  class  it  may 
be  stated  confidently  that  cerebral  hemorrhage,  usually  meningeal, 
is  the  cause  of  the  symptoms.  In  the  latter  class  it  is  probable 
that  an  intra-uterine  encephalitis  or  some  unknown  cause  has  pre- 
vented the  foetal  brain  from  developing. 

The  cases  which  have  developed  suddenly  after  birth  are 
cases  in  which  the  ordinary  causes  of  hemiplegia  in  adults  have 
been  acting,  and  must  be  traced  either  to  encephalitis,  hemor- 
rhage, or  embolism,  or  disease  of  the  vessels.  The  degree  of 
spontaneous  recovery  in  any  case  can  be  pretty  well  determined 
by  an  examination  at  the  end  of  the  second  year.  A  complete 
cure  never  occurs. 

The  fits  in  organic  epilepsy  are  likely  to  be  more  frequent 
and  severe  than  in  idiopathic  epilepsy ;  as  many  as  twenty  con- 
vulsions may  occur  daily  for  weeks  at  a  time.  These  fits  do  not 
destroy  life,  but  render  life  a  burden.  When,  however,  they  are 
infrequent  they  may  be  benefited  to  some  degree  by  the  use  of 
bromides. 

II.  The  second  class  of  cases  presents  mental  defects  more 
noticeable  than  physical  symptoms.     The  child  may  be  slow  in 


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DISEASES    OE    THE    NERVO'US    SYSTEM.  «1 

learning  to  talk,  may  soem  unable  to  tix  its  attention  upon  any- 
thing continuously,  may  be  exceedingly  active,  in  constant  mo- 
tion— the  activity  being,  however,  aimless ;  may  throw  things 
about,  or  tear  things  up,  or  put  everything  into  its  mouth  ;  may 
be  very  difficult  to  manage  because  of  its  inability  to  retain  and 
combine  impression.s  with  sufficient  power  to  reason  upon  them  ; 
and  mav,  therefore,  be  incapable  of  appreciating  the  meaning  of 
punishment,  if  this  be  inflicted.  Such  children  may  have  good 
powers  of  perception,  may  recognize  persons  and  objects,  show 
pleasure  at  bright  colors,  or  music,  or  caresses;  but  fail  to  show 
evidence  of  thought  in  the  sense  of  reasoning  power,  judgment, 
or  self-control.  Some  patients  constantly  drule  at  the  mouth, 
cannot  be  taught  cleanly  habits,  and  are  manifestly  imbecile. 
Other  patients  are  quite  bright  in  many  directions,  may  even  be 
precocious,  show  talents  in  music,  or  drawing,  or  fondness  for 
mathematics,  designing,  languages ;  yet  are  apparently  unable  to 
appreciate  moral  ideas,  cannot  be  taught  to  tell  the  truth,  are 
cruel  and  bad,  will  not  control  any  of  their  impulses,  and  so  are 
the  distress  and  despair  of  parents  and  teachers.  It  is  those 
mental  qualities  which  are  the  product  of  the  highest  evolution 
which  have  failed  to  develop  in  this  class  of  cases.  The  final  re- 
sult is  that  they  have  to  be  taken  care  of  all  their  lives,  either  at 
home  or  by  attendants,  being  incapable  of  supporting  themselves 
or  directing  their  conduct.  ^Nlany  of  them  have  epilepsy.  Some 
of  them  have  hemiplegia. 

III.  The  third  class  of  cases  is  less  common  than  the  two 
preceding,  and  is  likely  to  escape  observation  unless  carefully 
investigated.  The  patients  belonging  to  this  class  may  be  hemi- 
plegic  or  may  present  no  motor  or  mental  defects,  though  they 
may  be  the  subjects  of  epilepsy.  They  do  have  defects  of  sensory 
perception.  Such  defect  may  be  in  the  form  of  hemianopsia  or 
of_deafne^a.  It  is  probable  that  many  cases  of  deafmutism  belong 
to  this  class,  and  in  some  persons,  as  in  Laura  Bridgeman,  deaf- 
ness, dumbness,  and  blindness  coincide. 

The  pathological  changes  in  the  brain  in  these  various  cases 
dififer  widely,  and  are  as  follows,  in  the  order  of  frequency : 

Porencephalus,   a   localized   atrophy   or   agenesis,   leaving   a 


82  DISEASES    OF   THE    NERVOUS    SYSTEM. 

cavity  in  the  cerebral  hemisphere,  which  may  be  deep  enoug-h  to 
open  into  the  ventricle. 

Sclerotic  atrophy,  an  atrophic  condition  of  the  brain  with  an 
increase  of  connective  tissue  and  disappearance  of  the .  nervous 
elements  ;  affecting  both  hemispheres,  or  one  only,  or  a  part  of 
one  only ;  or  limited  to  small  areas  in  various  parts. 

Maldevelopment  and  apparent  atrophic  condition  of  the  mi- 
nute structures  of  the  hemispheres,  chiefly  cortical,  the  cells  re- 
sembling those  of  a  new-born  child,  but  with  no  apparent  gross 
defects  in  the  brain. 

Atrophy,  consequent  upon  the  condition  of  softening  pro- 
duced by  embolism  or  thrombosis,  and  limited  in  extent  to  certain 
arterial  districts  of  the  brain. 

M eningo-encephalitis,  a  condition  shown  by  thickening  and 
adhesion  between  the  pia  and  the  brain,  with  destruction  of  the 
cerebral  cells  and  atrophy  of  the  cortex. 

Cysts  lying  on  the  brain  and  producing  atrophy  by  pressure 
or  associated  with  atrophy  due  to  the  original  lesion  of  which  the 
cyst  remains  as  a  trace. 

Hemorrhage  on  or  in  the  brain,  as  shown  by  the  remains  of 
a  clot,  or  by  hgematin  staining  of  a  cyst,  of  the  pia,  or  of  the 
sclerotic  tissue. 

Hydrocephalus  with  extreme  dilation  of  the  ventricles,  so 
that  the  brain  tissue  is  reduced  to  a  mere  wall  about  the  cavity. 

These  are  the  conditions  found  at  death  in  cases  presenting 
the  clinical  features  just  studied.  It  is  evident  that  they  have  this 
in  common,  namely,  a  condition  of  atrophy  of  the  brain.  The 
origin  of  this  atrophy  is  not  always  clear.  In  some  cases  it  is 
clearly  congenital  and  due  to  a  maldevelopment  of  the  embryo. 

In  other  cases  it  is  clearly  traceable  to  injuries  at  births 
In  other  cases  it  must  be  ascribed  to  affections  of  various  kinds, 
such  as  inflammations  of  the  membranes  or  of  the  brain  sub- 
stance, or  vascular  lesions  and  their  consequences,  such  as  occur 
in  adults.  But  it  is  evident  that  the  various  processes  of  disease 
have  as  a  fairly  uniform  result  a  condition  of  atrophy  with  sclero- 
sis of  the  brain,  which  may  be  termed  sclerotic  atrophy.     The 


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DISEASES    OF    THE    NERVOUS    SYSTEM.  85J 

difference  in  the  clinical  types  is  clue  to  the  varying  situation  of 
the  lesion  rather  than  to  its  varying  nature. 

For  such  conditions  there  can  be  no  treatment. 

Tumors  of  the  Brain. 

J\iricfics  in  order  of  fre(iuency  : 

Gil  III  ma:  soft  gelatinous,  or  hard  cellular,  situated  on  base 
or  in  cortex,  usually  beginning  in  meninges. 

Tubercular:  hard  masses,  often  multiple,  especially  frequent 
in  children,  situated  anywhere,  sometimes  primary,  usually  sec- 
ondary. This  is  the  variety  in  more  than  one-half  the  cases  in 
children.     ^^  ^  i -^  - 

Glioina:  peculiar  to  the  nervous  system,  cells  and  fibres  like 
the  neuroglia,  usually  infiltratecp  and  without  boundaries,  but 
single^ .usually  vascular;  hence  symptoms  vary  and  hemorrhage 
occurs ;  usually  situated  in  the  white  substance. 

Sarcoma  of  all  varieties :  fibro-,  round-cell,  spindle-cell,  glio- 
sarcoma,  begin  from  connective  tissue  of  membranes  as  a  rule, 
sometimes  in  the  brain.  Hard  single  tumors,  of  various  sizes, 
easily  separable  and  well  defined,  situated  on  base,  in  meninges, 
in  cerebellum.  ''-^*'— u^zs  . 

Carcinoma:  rare,  usually  secondary. 

Occasional  varieties ^■d.r^t  fibromata,  osteomata,  psammomata, 
cholesteatomata,  angiomata.  lipomata,  ecchinococcus,  and 
cvsticercus.(''ew>t/<.^ut->-.^  ■^  ^1,^^—0.^  ^ 

.jjieurisms  of  the  base  give  rise  to  symptoms  of  tumor. 

For  Pathology  of  Tumcjrs,  see  Delafield  and  Prudden's  '-Pathology." 

Causes  of  Brain  Tumor. —  i.  Predisposing:  Sex:  males  twice 
as  freciuentlv  affected  as  females.     Age :  children  most  liable,  as 
tubercular  tumors  are  frequent.     Young  adults  next.     Old  age  ^..^-tA.  * 
is  quite  exempt,  except  from  carcinoma. 

2.  Exciting.  Injuries.  Severe  emotional  shock.  Unknown 
in  large  majority. 

Situation. — Cerebral  cortex.  twcnt\-five  per  cent. ;  cerebel- 
lum, twent}-five  per  cent.  ;  centrum  ovale,  fifteen  per  cent. ;  basal 


84  DISEASES    OF   THE    NERVOUS    SYSTEM 

ganglia,  ten  per  cent. ;  pons,  ten  per  cent. ;  crus  and  corpora  quad- 
rigemina,  ten  per  cent.     Others,  five  per  cent.  Qw.j!>m^") 

Effects  of  Brain  Tumor. — i.  Direct  effects.  Irritation  of 
gray  matter  with  nervous  discharges,  and  destruction  of  brain- 
tissue.   (Uuuu-^-J^     «   /a.4«.,-.^^t^^-tX--v    -1    ^^....^.U^^    .   'Pvo-cC^t*  iUrx:-JL  'i.^y^^.^^yi^Z^ 

^  2.  Indirect  effects.  General  pressure  on  entire  brain.  This 
may  be  hmited  by  the  falx  or  tentorium.  It  produces  hydroceph- 
akis  by  pressure  on  ventricle  or  veins  of  Galen.  Vascular  dis- 
turbance by  pressure  on  arteries  and  veins.  Meningitis,  localized 
and  not  purulent,  except  in  tubercular  cases.  Thinning  of  cra- 
nial bones. 

Effects  of  increased  pressure  are  seen  after  death  in  flatten- 
ing of  the  convolutions,  anaemia  and  pallor  of  the  brain,  dry  sticky 
state  of  membranes,  and  distension  of  ventricles  by  serum. 

Symptoms  of  Brain  Tumor. — I.  General  symptoms  depend 
on  existence  of  a  new  growth  independent  of  its  position.  cUm-./ 

Headache  in  ninety^fiye^ per  cent.,  constant  or  intermittent; 
general  or  local ;  dull  and  deep,  increased  by  anything  which  de- 
ranges the  cerebral  circulation. x  Sometimes  head  is  tender  to 
percussion  at  certain  points ;  may  have  evidence  of  pain  even  in 
state  of  stupor ;  it  may  be  agonizing ;  it  may  give  feeling  of  band 
about  head ;  it  is  often  worse  at  night,  causing  insomnia,  espe- 
cially in  gumma. 

Mental  disturbance,  eighty-five  j>er^ent.  Dulness  and 
apathy,  with  imperfect  attention  and  memory.  Depression  and 
emotional  state.  Slow  speech,  gradual  mental  failure,  childish- 
ness,, and  dementia ;  fainting  attacks,  stupor,  and  coma  in  the  last 
stage.     Occasionally  delirium  and  active  insanity. 

Optic  neuritis,  eightv  per  cent  Venous  congestion.  Swell- 
ing of  papilla,  loss  of  disc  outline ;  radiating  appearance  about  the 
disc  and  hemorrhage ;  then  optic-nerve  atrophy  leaving  white  or 
gray  disc.  In  cases  of  subcortical  tumor  of  small  size  it  may  be 
absent.  Sight  may  be  affected ;  visual  field  small  and  irregiilar, 
or  unimpaired  for  a  time. 

Vertigo  or  sense  of  giddiness,  frequent  in  tumors  in  posterior 
fossa.  May  occur  in  tumors  anywhere  on  change  of  position. 
May  be  due  to  paralysis  of  one  or  more  ocular  muscles.     CUjujua.x«  ejxJ2^ 


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DISEASES    OF    THE    NERVOUS    SYSTEM.  H5 

\'omiting.  with  or  without  nausea  or  relation  to  food.  l''re- 
quent  in  tumors  in  posterior  fossa.      ^  Ta^^^^  "^1^+^ 

General  convulsions  of  cpile])tic  type.  Petit  iiial  or  t^rand 
mal. 

Xvstagmus.  lateral  oscillation  of  eyes.  Frequent  in  disease 
of  corpora  quadrig-eniina  and  cerebellum.     ^^•-^■^  r-e.^^.^.^   ^i,*^  Ju,*.,,. 

Loss  of  control  over  sphincters  occurs,  especially  with  tumors"- 
in  the  frontal  lobes. 

Glycosuria  and  polyuria,  especially  with  tumors  in  the  pos- 
terior fossa. 

Slow  fiulse  :  50  to  60. 

II.  Local  symptoms  dependent  upon  the  position  of  the 
tumor. 

Frontal  Lobes:  Mental  dulness.  lack  of  control  of  emotions, 
irritability,  inattention,  and  childishness,  dementia,  loss  of  sense 
of  smell,    <v!<^sl/a    ^1  OvwCw^    -^  s-^f^^^^Mi^^  . 

Left  third  frontal  convolution.     Motor  aphasia. 

Central  Convolutions,  and  motor  tra.d:.  ^^lonospasm  and 
monoplegia  when  in  or  near  cortex.  Hemispasm  and  hemiplegia 
when  deep  or  in  capsule.  Sometimes  slight  ansethesia  in  para- 
lyzed part. 

Occipital  Lobe  and  visual  tract.  Hemianopsia,  noticed  by 
patient  as  unilateral  blindness.  Visual  hallucinations  and  flashes 
of  light  on  one  side. 

T.eft  Teiijj)oral  lirst  and  second  cojTyoliiiions^__  Sensory 
aphasia:  form,  \yord-deafness.      '?'yy^^(yiy^.j^..i,c^  •     ■<!A.ctc:czt.^yvKU  ^^vL—^ 

Left  Lozi^'er  Parietal  lobule  and  angular  gyrus  or  in  occipito- 
temporal tract.     Sensory  aphasia:   form,  word-blindness. 

Base  of  brain. 

Anterior  fossa :  Loss  of  smell. 

Aliddle  fossa :  Hemianopsia,  paralysis  of  ocular  muscles.  III., 
IV.,  \^I. ;  neuralgia  of  face  and  ansethesia,  V. ;  paralysis  of  III. 
and  opposite  hemiplegia,  neuroparalytic  ophthalmia,  nystagmus  ; 
bilateral  spastic  paralysis,  deafness. 

Posterior  fossa :  Paralysis  of  \'II.,  IX.,  X.,  XI.,  XII. ;  vertigo 
and  aural  symptoms ;  cerebellar  ataxia,  tendency  to  one  side ; 
paralysis  ^yidespread  from  medulla  disease. 


"u*.  "^.^    (Uy<£^^K 


86  DISEASES    OF    THE    NERVOUS    SYSTEM. 

Cerebellum  :  A'ertigo,  vomiting,  cerebellar  ataxia  when  mid- 
dle lobe  is  involved ;  headache,  frontal  or  occipital  and  severe  ; 
optic  neuritis  early. 

Dia_!::;nosis. — Cerebral  symptoms :  g;eneral  alone,  or  general 
and  local,  point  to  the  presence  of  a  tumor. 

Differentiation  from  chronic  nephritis  :  By  examination  of 
urine ;  bv  condition  of  heart,  arteries,  and  blood-pressure ;  by 
appearance  of  optic  disc  and  retina  in  many  cases,  hemorrhages 
more  frequent  and  white  spots  far  from  disc  :  by  character  of 
headache,  more  severe  in  tumor ;  by  age  of  patient,  young  per- 
son =  tumor. 

From   hypermetropia    with    astigmatism   and    angemia,    W2th_ 
menstrual  disorder  :   By  examination  of  eyes  and  relief  by  glasses  ; 
by  cure  of  ansemia  by  diet.  iron,  and  aloes  :  by  slight  degree  of 
headache  and  neuritis. 

From  hvsteria  with  migraine  :  By  study  of  the  patient  and 
separation  of  real  svmptoms  :  by  condition  of  the  optic  disc. 

From  abcess :  By  history  of  trauma  or  of  otitis  media  ;  by 
severity  of  early  symptoms  in  abscess ;  by  fever  in  abscess ;  by  late 
development  of  optic  neuritis,  rare  in  abscess. 

To  determine  the  location :  Study  carefully  the  local  symp- 
toms, "signal  symptom.""  c.  g.,  numbness  and  twitching  of 
thumb.  Study  also  the  order  of  appearance  of  local  symptoms : 
thumb,  hand,  face.  Compare  the  several  local  symptoms,  paral- 
ysis -j-  aphasia,  or  -j-  hemianopsia. 

To  determine  the  vai'iety :  Estimate  probable  frequency  of 
various  tumors  at  different  ages.  Look  for  history  of  syphilis, 
tuberculosis,  cancer,  or  sarcoma.  Study  rapidity  of  onset ;  gli- 
oma, tubercle,  cancer  are  rapid.  Study  signs  of  irritation ;  more 
frequent  in  glioma  and  meningeal  tumors.  Study  signs  of  varia- 
tion in  severity  of  symptoms  ;  more  variation  in  glioma.  Study 
situation  of  the  tumor ;  basal  tumors  are  often  gumma,  tubercle 
sarcoma.  Intracerebral  tumors  are  often  glioma,  sarcoma.  Pecul- 
iar forms  of  hemiopia  and  earh-  optic  neuritis  indicate  sarcoma 
of  pituitary  body  or  aneurism. 

Course  of  the  disease :  Begins  with  general  symptoms 
usually.  Sometimes  begins  with  local  spasm  or  a  general  con- 
vulsion.    (Gradual  increase  in  severity  and  number  of  symptoms. 


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DISEASES    OF    THE    NERVOUS    SYSTEM.  ^<T 

Finally  death  in  stupor  or  in  general  convulsion  or  suddenly, 
from  heart  failure,  or  recovery  under  specific  treatment. 

Duration  is  from  one  to  three  years. 

Prognosis,  bad,  excepting  in  gumma  and  when  tunnjr  can  be 
removed. 

Treatment. — For  gumma  :  Inunctions  of  mercury  and  KI  to 
three  hundred  grains  daily.  '^SvSLr^^y^t^^  ^^U^a^w^-w..^  ^  imJX^^'^^t^)) 

Surgical  treatment :  Removal  is  possible  when  diagnosis  of 
location  is  exact.     There  is  danger  of  return. 

For  Cranio-Cerebral  Topography,  see  page  40. 

Abscess  in  the  Braix.         kuJL^-^^^^*^^    >a/-^l.^-c4,&. 

Acute  encephalitis  with  formation  of  pus  results  in  an 
abscess.  (I )The  abscess  may  extend  rapidly,  not  being  encapsulated, 
and  cause  death  izpr  it  may  become  encapsulated  and  develop 
slowly,  oif^Jbecome  stationary  and  remain  for  years  as  a  foreign 
substance  producing  no  symptoms,  but  finally  enlarge  or  break. 
(41  Occasionally  multiple  abscesses  develop  in  the  brain  secondary  to 
,-f  pyaemia,  producing  cerebral  symptoms  in  the  course  of  that  dis- 
ease.    There  may  be  a  secondary  meningitis  in  either  form. 

Sitiiafwii. — Is  usually  in  the  temporo-sphenoid  lobe  or  in  the 
frontal  lobe  or  in  the  ^erebeUiuiL  in  the  white  matter. 

Causes. — Chronic  otitis  media,  forty  per  cent.  Fracture  of 
cranial  bones,  thirty-five  per  cent.  Chronic  rhinitis,  ten  per  cent. 
Caries  of  anv  cranial  bone,  ten  per  cent.  Secondary  to  infectious 
diseases,  five  per  cent. 

Sxniptoiiis.^After  an  injury  or  after  otorrhcea  or  other  cause 
cerebral  symptoms  develop  suddenly  ;  severe  headachy  vomiting, 
mental  distress  and  dulness,  stupor,  a  chill,  a  high  temperature 
for  a  day  or  t\va^;  leucocytosis,  possibly  convulsions  ;  rarely  local 
symptoms  ;  hemiplegia,  hemianopsia,  aphasia,  cerebellar  stagger- 
ing. In  a  week  the  patient  is  very  ill,  with  irregular  tempera- 
ture, sometimes  with  chills,  sometimes  no  fever ;  slow  pulse ;  in- 
tense pain,  delirium,  stupor,  and  optic  neuritis.  If  abscess  ex- 
tends death  follows  in  two  weeks,  or  suddenly  from  rupture.  If 
abscess  discharges  into  ear  or  nose,  or  if  it  can  be  opened,  symp- 
toms  subside.      Rarel}'   symptoms   suliside   spontaneously   slowly, 


88 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


the  abscess  becoming  encapsulated  and  latent,  and  patient  appar- 
ently recovers,  but  is  subject  to  headache  and  vertigo;  and  has 
a  relapse  later. 


Diagnosis. — 

Abscess 

Temperature.normal  or  not  high. 
Pulse  slow. 
Patient  in  stupor. 

Spasms  and  rigidity  rare. 
Cranial  nerves  not  involved. 
Optic  neuritis  frequent. 

Abscess 

Temperature  normal  or  not  high. 

Pulse  slow. 

Chill  at  onset  not  repeated. 

Little  sweating. 

Head  tender  to  percussion? 


vs.  Meningitis. 

Temperature  high  without  remission. 
Pulse  rapid.  * 

Patient    irritable,    all     senses    over- 
acute. 
Spasms  and  rigidity  frequent.     Ka->^-<--l-s   -r 
Cranial  nerves  involved  early.  -*-  'vi-^om^c^  >a  Aju-- 
Optic  neuritis  rare.  i  -  i 

z's.     Thrombosis  of  Later.\l   Sinus. 

Temperature  high  with  remissions. 
Pulse  rapid,  weak. 
:ir  Chills  frequently  repeated. 
Profuse  sweating. 
Pain  over  mastoid  and  jugular. 
Thrombi  in  lungs. 


Diagnosis  of  location  is  made  parti v  from  the  exciting  cause 
and  partly  from  the  local  symptoms. 

Prognosis  fatal,  unless  abscess  can  be  opened. 

Treatment. — In  the  few  cases  in  which  the  abscess  can  be 
located,  operation  of  trephining  and  drainage. 


Cerebro-spinal  Sclerosis. 

Multiple  or  disseminated  sclerosis  is  a  rare  disease  affecting 
the  brain  and  spinal  cord  together.  Small  regions  of  sclerotic 
tissue  are  found  irregularly  scattered  through  the  entire  nervous 
system,  without  destruction  of  the  axis  cylinders  of  the  nerve- 
tracts.     Its  cause  is  unknown. 

Symptoms. — Headache,  vertigo,  malaise,  mental  irritabilitv,. 
inattention,  imperfect  memory,  lack  of  self-control,  and  inability 
to  work.  Later,  tremor  of  hands  increased  by  an  effort  to  hold 
them  still,  nystagmus,  increased  knee-jerk,  stiff  spastic  gait,  weak^ 
ness,  and  finally  general   tremor  on   effort.     Slow   speech,   each 


.  ^--«=l'''K,t-X7 


DISEASES    OF   THE    NERVOUS    SYSTE^r.  8^ 

syllable  separately  eiiunciated  without  variation  of  tone.  Optic 
atrophy.  Dementia  and  attacks  of  epilepsy  and  hemiple.c^ia  may 
finally  occur. 

Course  is  exceedingly  irregular,  symptoms  may  disappear  for 
months  and  then  return.  The  disease  is  often  mistaken  for 
hysteria. 

Diaj^niosis  is  made  by  excluding  all  other  organic  diseases, 
by  nystagmus,  tremor,  and  speech. 

Treat inait. — Arsenic  -gV  gr.  daily;  solanin  14  gr.  daily, 
increased. 

Syphilis  of  the  Brain. 

Syphilitic  afifections  of  the  nervous  system  may  be  produced 
by: 

1st.   Syphilitic  endarteritis. 

2d.  Direct  action  of  the  syphilitic  poison  upon  the  nervous 
system. 

3d.   Syphilitic  exudations  in  the  meninges. 
.    4th.   Syphilitic  deposits  in  the  brain  itself. 

5th.  Hereditary  syphilis. 

I  St.  Syphilitic  endarteritis  produces  a  progressive  diminu- 
tion in  the  calibre  of  the  blood-vessels,  resulting  in  a  state  of 
anaemia,  malnutrition  of  the  brain  supplied  by  the  vessels  afifected, 
and  leads  to  thrombosis  followed  by  localized  softening  in  the 
area  cut  off  from  its  blood  supply.  The  symptoms  of  this  condi- 
tion are  in  the  early  stage  those  of  malnutrition  of  the  brain  and 
imperfect  action  in  the  regions  afifected.  The  patients  present  at 
first  symptoms  of  neurasthenia,  and  later  slight  temporary  sus- 
pension of  functions,  such  as  temporary  aphasia,  numbness  in  one 
limb  or  in  one-half  of  the  body,  a  condition  of  weakness  not 
amounting  to  paralysis  in  one  limb  or  one-half  of  the  body, 
double  vision,  or  vertigo.  Stimulants  to  the  heart  relieve  these 
symptoms,  but  after  a  time  if  a  thrombosis  occurs  the  symptoms 
of  cerebral  apoplexy  suddenly  appear.  After  such  an  apopletic 
attack  a  partial  recovery  may  ensue,  but  as  a  spot  of  softening 
in  the  brain  is  usually  left,  a  complete  recovery  is  not  to  be  ex- 
Dected ;  hence  the  fact  that  a  syphilitic  lesion  which  can  be  re- 


■yO  DISEASES    OF    THE    NERVOUS    SYSTEM. 

moved  bv  treatment  is  the  cause  of  the  apoplectic  attack  does  not 
warrant  a  more  favorable  prognosis  in  such  cases. 

2d.  The  toxic  effects  of  syphilis  on  the  nervous  system  are 
manifested  by  general  disturbances  of  function,  which  produce 
the  symptoms  of  neurasthenia  of  all  the  various  types.  As  a  rule, 
in  syphilitic  neurasthenia  the  symptoms  appear  to  be  worse  to- 
ward evening  and  insoinaia.  is  more  persistent  than  any  other 
symptom ;  hence  in  general  neurasthenia  with  insomnia  any 
syphilitic  element  must  be  looked  for  and  treated  before  the 
neurasthenia  can  be  cured.  Neurasthenia  may  occur  in  syphilitic 
persons  without  any  direct  connection  with  the  syphilis,  which  at 
the  time  may  be  latent.  A  test  of  treatment  is  the  only  one  en- 
abling differential  diagnosis  to  be  made. 

3d.  Syphilitic  exudations  into  the  meninges  of  the  brain  and 
syphilitic  meningitis  are  exceedingly  common  as  a  sequel  of  syphi- 
litic disease.  From  two  to  ten  years  after  the  infection  gummy 
-exudations  may  occur  in  any  part  of  the  brain,  but  are  more  fre- 
quent upon  the  base  of  the  brain  and  about  the  crus  and  pons. 
The  glue-like  substance  is  deposited  rapidly  and  extensively 
through  the  meninges,  producing  pressure  upon  the  subjacent 
brain  or  upon  the  cranial  nerves,  and  thus  causing  suspension  of 
function  in  the  parts  compressed.  Occasionally  the  syphilitic  ex- 
udation takes  the  form  of  a  hard  tumor,  which  then  produces  the 
regular  symptoms  of  tumor  of  the  brain.  The  symptojiis  of  — 
syphilitic  gumma  or  syphilitic  basilar  meningitis  are  headache.  "^ 
worse  at  night,  insomnia,  mental  irritability,  vertigo,  distressing 
sensations  in  the  head,  occasional  vomiting,  and  local  symptoms 
of  paralysis  of  the  cranial  nerves,  the  third  and  sixth  being  the  N^ 
■ones  particularly  affected.  If  the  exudation  is  not  upon  the  base, 
•or  occurs  in  the  convexity  or  over  the  cerebellum,  the  local  symp- 
toms will  be  those  of  irritation  or  of  arrest  of  function  of  the 
particular  portion  of  the  brain  affected.  Thus  spasms  and  paral- 
ysis, paraesthesia  and  ansethesia,  hemiopia,  or  any  variety  of 
aphasia  may  be  caused  by  the  disease.  The  pressure  upon  the 
vessels  produced  by  syphilitic  exudations  adds  to  the  complexity 
of  the  symptoms.  Convulsions  are  frequently  observed  in  such 
cases,  both  of  a  general  and  of  a  local  tyP^-  Increased  thirst  and 
hunger  and  polyuria  are  often  found.     The  course  of  the  case 


\_,^ '        Catfu«>u.MA      'H'        S^'fe-^X  ira^A-oLoJC^"  (r^4J2!Li_iL_^     c6c^i_G4^     c-,^ 

OU  i^U^    (>o-e_.ui-    -T-cJV     0-^sji-»^  ~t5  ^  '^'-'-^     cnrt!oi-c    iz^XSI^CAA^-ai^^f", 

~T~fiC>^^   rW^'^-i^  (J-^.J2^J2<^  ^\ 
A   /Wi>^^^J^    S^^-o.-^      V^^^i.^     /^Ji^.^xJ::^    Ia^  C^./L.rC;i     Ko^  ^^-^  ■ 
QjL^M^  JUrt^    cjM.    ^     '^-^t^  ■    -^-»^    Ova     O^    /<^<:^^c    '4       r^^^^  - 

GaaJU-o^-    feoc^J)-  fW'iL    Ax4^.     (|^<xt-  x^SX^    Uo-b     <«^^«-^ 

X. 


DISEASES    01'    Till'".    XKRVOUS    SYSTEM.  91 

IS  more  rapid  in  its  onset  than  that  of  brain  tumor,  but  resembles 
it  in  all  other  respects  and  may  be  associated  with  optic  neuritis. 
The  symptoms  sul)si(le  rapidlx'  under  inunctions  of  mercury  and 
large  doses  of  iodide  of  potash,  and  hence  prognosis  is  good  in 
the  majority  of  cases,  though  relapses  are  frequent. 

4th.  Syphilitic  deposits  in  the  brain  itself  may  be  of  the 
nature  of  small  dessimated  spots,  producing  chronic  indurative 
or  sclerotic  processes  of  small  regions  of  softening.  The  symp- 
toms of  this  afifection  are  identical  with  those  of  general  paresis, 
and  can  only  be  distinguished  from  paresis  by  the  result  of  treat- 
ment. 

5th.  Hereditar}'  syphilis  occasionally  produces  the  symptoms 
of  cerebral  atrophy  or  the  symptoms  of  multiple  cerebro-spinal 
sclerosis  in  children,  and  in  either  of  these  conditions  this  fact 
must  be  kept  in  mind,  and  if  other  signs  of  hereditary  syphilis  are 
discovered  this  element  must  be  considered  in  the  treatment. 

1  •  Aiuft^.Jt«_..^.*_*^  -^icJiZ^^^^^CU^  (/-oc^t^-f-i:,,^  .CL^^'^cc'i 

C    .  ^rW-**-    '1     wCJL-J^,     ^Vl>N»-^M"    cu,*_^^~  /x..  cL^  a*«a-U:T'    ftv^-v^,     /^--•--^U  cx-i^ 


FUNCTIONAL    NERVOUS    DISEASES. 
Neurasthenia. 

Nervous  prostration,  nerve  tire,  nervous  irritable  weakness 
is  a  functional  disease  of  the  entire  nervous  system,  brain,  spinal 
cord,  spinal  and  sympathetic  nerves,  dependent  upon  malnutri- 
tion, characterized  by  nervous  weakness  and  irritability. 

A  balance  between  expenditure  of  energy  and  nutrition  must 
be  preserved. 

Brain  overwork  or  anxiety ; 

Spinal  cord  overwork  by  long  marches  or  sexual  overaction. 

Nerve  overwork  by  various  occupations  in  which  a  single  act 
is  repeated ; 

Vasomotor  work  in  maintaining  vascular  tone  and  nutritive 
processes,  all  require  a  sound  basis  and  rest  at  periods. 

When  balance  between  store  and  expenditure  of  energy  is. 
broken,  exhaustion  results.  Then  nature  enforces  rest  by  fatigue^ 
by  sleep.  One  may  disregard  nature,  but  if  so  one  must  pay  the 
penalty. 

Causes. — I.  Excessive  expenditure  of  nerve  energy. 

Primary  neurasthenia  more  common  than  secondary. 

Influences  favoring  its  production  : 

1.  Bad  hereditary  influences.    Weak  nervous  system. 

2.  Feebleness  in  childhood,  with  poor  nervous  system. 

3.  W^rong  methods  of  training  and  education. 

4.  The  struggle  for  existence.     Kant's  rule,  eight  hours 

for  work,  eight  hours  for  diversion,  eight  hours  for 
sleep. 

5.  Anxiety,  worry,  mental  depression,  fear. 

6.  Mental  or  physical  overwork. 

7.  Sexual  excesses. 

II.  Deficient  supply  of  nervous  energy. 
Secondary  neurasthenia. 


DISEASES    OF   'J"HE    NERVOUS    SYSTEM.  93 

inrtuences  favoring  its  production  : 

1.  Weakening  diseases  of  all  kinds  of  organic  nature. 

2.  Indigestion    and    dyspe]->sia,    with    auto-infection    by 

products. 

3.  Gout,  rheumatism,  uric-acid  diathesis. 

4.  Infectious  diseases,  typhoid,  grippe,  malaria. 

5.  Alcoholism  or  abuse  of  drugs. 

Result  of  the  action  of  these  causes  is  to  produce  malnutri- 
tion of  the  nervous  system  and  state  of  irritable  weakness. 

1.  The  power  of  continuous  activity  is  impaired;  weakness 
results ;  hence,  mental  work  is  imperfect ;  attention  flags ;  mem- 
ory fails ;  ambition  ceases ;  physical  activity  is  imperfect ;  exer- 
cise tires  one ;  lassitude ;  vegetative  functions  are  impaired.  Di- 
gestion is  poor ;  constipation  occurs ;  vascular  tone  is  impaired ; 
heart  feeble.  Balance  must  be  maintained  between  blood  supply 
and  functional  activity.  When  this  is  impaired  work  is  impossi- 
ble.    Secretions  are  changed  in  amount  and  character,  e.  g.,  urine. 

2.  The  power  of  mental  and  physical  control  is  impaired  and 
irritability  results ;  inhibition  may  be  partly  automatic  and  partly 
conscious ;  it  must  be  conscious  and  voluntary  to  prevent  morbid 
fear  and  apprehension ;  influence  of  fear  is  to  inhibit  all  nervous 
acts — e.  g.,  walking  on  ice,  oral  examination,  stage  fright ;  this 
control  is  weakened,  and  hence  irritability  results. 

Symptoms  of  Neurasthenia. — 

1.  Cerebral:  Headache — dull,  occipital,  frontal;  sensitiveness 
of  scalp ;  vertigo  ;  insomnia  ;  cerebral  sensations — fulness,  band, 
pulsation. 

2.  Mental :  Apprehension — morbid  fears,  of  places,  people, 
solitude,  etc. ;  inattention  and  forgetfulness ;  incapacity  for  work ; 
idiosyncracies  become  prominent ;  irritability  of  temper  ensues ; 
anxiety  and  exhaustion ;  imperfect  respiration  and  rapid  pulse. 

3.  Spinal :  Pain,  especially  in  nape  of  neck  and  sacrum ; 
irritation ;  hypersensitiveness ;  sensitiveness  about  ribs  and  inter- 
costal nerves ;  weakness,  legs  give  out ;  sexual  irritation,  erections, 
impaired  power ;  emissions ;  bladder  irritability,  frequent  mic- 
turition. 

4.  Vasomotor :   Flushes,  cold  extremities ;  undue  sweating : 


94  DISEASES    OF    THE    NERVOUS    SYSTEM. 

transient    blueness    or    oedema;    tache    ccrchrale    of    Trousseau; 
tachycardia ;  palpitation. 

5.  Gastro-intcstinal :  Indigestion  and  dyspepsia,  especially 
acid  stomach ;  imperfect  liver  action ;  constipation ;  pseudomem- 
branous colitis  ;  distension  of  abdomen  with  gas. 

6.  Sensory  and  motor  symptoms  :  Indefinite  pains  and  par?es- 
thesia ;  joint  affections;  apparent  paralysis — no  change  in  electric 
activity ;  vision  imperfect ;  asthenopia ;  visual  field  may  be  re- 
tracted.   Other  senses  rarely  affected ;  tinnitus. 

Diagnosis  made  by  the  existence  of  a  cause ;  the  absence  of 
objective  signs  of  organic  disease;  the  temperairr^nt  of  the 
patient;  the  variability  of  symptoms;  the  dispropott'on  between 
complaint  and  actual  power. 

Treatment. — Absolute  necessity  of  establishing  ncrve-energ}' 
by  restoring  balance  between  store  and  expendirure.  Hence 
supply  nutritive  elements  to  nervous  system  by  p-opcr  food,, 
properly  digested;  by  increasing  circulatory  power;  by  exercise; 
by  hydrotherapy;  by  massage;  and  diminish  exper.fl.'ture  of 
nervous  energy  by  rest,  if  necessary  absolute,  and  by  diveision. 

Direct  treatment  may  be  by  tonics  of  all  kinds ;  by  sedativcs,^ 
if  patient  is  extremely  nervous;  by  electricity;  £alvan>.s,n.  Treat 
symptoms  only  when  absolutely  necessary.  C-jmbat  the  desir*:  of 
these  patients  for  drugs,  and  their  depcud-nce  on  stimujrmts  and 
opiates. 

Hysteria. 

A  functional  disturbance  of  the  nervous  system  characterized' 
by  mental  and  moral  perversion,  lack  of  self-conrtol,  and  dis- 
orders of  any  or  all  the  bodily  functions. 

Women,  between  fifteen  and  twenty-five  years,  or  at  an}-  age.. 

Men,   at   an}-   age,    and    even   children,   may   be   affected. 

Causes. — Hereditary  inHuence  very  marked ;  malnutrition 
of  the  nervous  system  from  anaemia ;  indigestion ;  from  bad 
habits  of  life;  emotional  excitement;  fear,  anxiety,  jealousy; 
tendenc}-  to  imitation  }ielded  to  ;  epidemics  of  hysteria  ;  uterine 
and  ovarian  irritation  is  a  rare  cause.  Traumatism,  especially 
accidents  attended  bv  great  fear.     Several  causes  mav  concur. 


S6  DISEASES    OF    THE    NERVOUS    SYSTEM. 

tional  strain ;  scream,  convulsion,  opisthotonus,  facial  expression, 
series  of  short  attacks,  fit  of  crying,  passes  water,  cataleptic 
rigidity,   hysteroepilepsy. 

The  character  of  the  symptoms  varies  greatly.  The  symp- 
toms appear  and  disappear  suddenly. 

The  course  of  the  disease :  Chronic  condition  with  periods  of 
intensity ;  cure,  sudden  and  marvellous  ;  great  variation  in  symp- 
toms ;  very  rarely  death  in  convulsion  or  from  suicide. 

Diagnosis  is  never  made  from  a  single  symptom,  but  from 
a  study  of  the  general  condition. 

Treatment. — Mental  change  and  moral  education;  h3'dro- 
therapy ;  the  rest  cure  ;  mental  therapeutics  ;  tonics,  strychnine, 
iron,  and  quinine. 

Symptomatic   remedies : 

Sedatives  for  the  nervous  state,  bromides,  valerian,  laven- 
der, asafoetida.  Opium  is  to  be  avoided,  for  habit  is  easily 
formed. 

For  convulsion,  prevent  injury,  don't  use  chloroform,  use 
cold  water,  hold  patient,  stop  respiration,  don't  press  ovaries, 
give  emetic. 

For  faints,  irritation  over  heart  by  ice,  internally  spirits 
ammonia,  or  lavender. 

For  spasms,  hot  or  cold  applications,  cautery. 

For   paralysis,    electricity,   especially   faradism. 

For  pain,  hypodermics  of  water  after  one  of  morphine,  local 
applications  of  sedatives. 

Epilepsy. 

Epilepsy  is  a  functional  neurosis  characterized  by  sudden 
transient  loss  of  consciousness  with  spasmodic  actions  of  the 
muscles. 

There  are  three  varieties. 

(i)  Petit  nialj  in  which  the  loss  of  consciousness  is  very 
brief  and  the  spasm  slight  or  absent. 

(2)  Grand  mal,  in  which  there  is  a  coma,  a  general  convul- 
sion, with  biting  of  the  tongue,   frothing  at  the   mouth,  some- 


<s6<_-^. 


DISEASES    OF    THE    NERVOUS    SVSTE^r.  97 

times  involuntary  micturition,  and  a  general  weakness  and  a 
deep  sleep   following  the  coma. 

(3)  Psychicp.l  attacks  in  which  a  sudden  mental  aberration 
occurs  with  acts  of  violence,  or  odd  actions  lasting  several 
hours  or  even  days.  In  all  the  varieties  the  patient  is  uncon- 
scious during  the  attack,  no  matter  what  he  does,  has  after- 
ward no  memory  of  what  occurred  in  the  attack,  and  is  often  un- 
aware that  he  has  had  any  attack  at  all. 

Etiology. — It  is  more  common  in  males  than  in  females.  It 
is  a  disease  of  early  life,  but  no  age  is  exempt.  Many  cases 
can  be  traced  to  some  injury  or  organic  disease  of  the  brain  in 
infancy  or  childhood.  Any  organic  brain  disease  may  cause 
epilepsy  in  adult  life.  It  is  a  frequent ,«equal  of  injuries  of  the 
head  or  brain.  It  is  also  of  toxic  origin :  chronic  alcoholism, 
lead  poisoning,  tobacco  poisoning,  syphilis,  or  any  of  the  in- 
fectious diseases  may  be  followed  by  epilepsy.  In  nervous  chil- 
dren intestinal  toxaemia  may  cause  it.  Peripheral  irritation  long 
continued  in  a  very  nervous  person  may  cause  it ;  e.  g.,  foreign 
lx)dies  in  the  nose  or  ear,  irritation  of  teething,  adenoids  in  the 
throat,  phimosis,  painful  scars.  In  the  majority  of  cases  no 
cause  can  be  found.  In  the  aged  arterial  sclerosis  and  multiple 
areas  of  cerebral  softening  are  a  cause. 

Theory  of  the  Disease. — The  nerve  cells  store  up  energy 
which  is  liberated  in  any  act  of  mind  or  will  in  a  moderate  de- 
gree and  is  accompanied  by  sensations  or  muscular  acts.  In 
epilepsy  it  is  supposed  that  this  energy  is  suddenly  liberated  with- 
out moderation  and  hence  sensations  are  forced  upon  conscious- 
ness (the  aura)  and  muscles  are  thrown  into  violent  action 
( the  convulsion ) .  All  expenditure  of  nerve  energy  is  followed 
by  exhaustion  until  the  supply  is  renewed.  Hence  the  coma, 
sleep  and  weakness  following  the  attack.  The  reason  why  nerve 
cells  in  some  persons  are  ready  to  discharge  their  energy-  spon- 
taneously or  on  slight  provocation  is  unknown.  Any  mental  or 
physical  strain  is  capable  of  setting  off  the  explosion.  ^lany 
poisons  in  the  blood  are  also  capable  of  doing  so.  The  reason 
bromide  and  other  sedatives  check  the  disease  is  because  they 
reduce  the  tendency  to  the  sudden  discharge. 


98  DISEASES    OF   THE    NERVOUS    SYSTEM. 

Symptoms. — The  attack  is  often  preceded  by  some  sen- 
sation, a  numbness,  gastric  sensation,  a  vertigo,  a  flash  of  hght, 
a  sound,  a  fixed  idea.  This  is  called  an  aura.  It  is  an  indi- 
cation of  the  organ  of  the  body  or  of  its  corresponding  region 
of  the  brain  in  which  the  irritation  begins.  The  convulsion 
may  be  general  or  localized  in  one  part,  of  the  latter  it  indicates 
some  irritation  in  the  motor  area  of  the  brain.  Thus  many 
tumors  begin  with  a  local  spasm  or  a  general  fit.  The  attack  is 
followed  by  a  sleep  which  is  evidence  of  exhaustion  of  the  brain. 
Every  possible  variation  in  the  severity  of  attack  from  a  petit 
mal  of  an  instant's  duration  to  a  grand  mal  of  many  hours  has 
been  observed.  When  a  series  of  grand  mal  attacks  occur  the 
condition  is  termed  status  epilepticus.  This  is  the  only  danger- 
ous form,  as  death  rarely  occurs  in  an  attack.  The  pupils  oi 
epileptics  are  always  dilated  and  though  they  contract  again 
dilate  in  light.  The  memory  becomes  poor  as  the  disease  goes 
on.  Judgment  is  impaired.  A  final  state  of  dementia  is  ob- 
served in  many  cases. 

Prognosis. — Recoveries  are  rare.  The  disease  is  chronic, 
but  the  intervals  between  attacks  may  be  lengthened  by  treat- 
ment.      ^^Ooo^U-b^    ^  i    :AJbtT>-et— >    t»    7  y^"^   o_>j^v,r2c^ 

Treatment. — A  simple  diet  from  which  meat  is  almost  ex- 
cluded. Suflicient  amount  of  bromide  of  potassium  and  sodium 
and  ammonium  combined  to  hold  attacks  in  check,  given  on 
rising  and  at  bed  time  well  diluted.  Other  remedies  are  tincture 
of  simulo,  one  teaspoonful ;  antipyrin,  15  grains;  solanum 
carolinense,  20  drops ;  chloral,  10  grains ;  Belladonna,  Digitalis. 
Heart  tonics  may  be  combined  vAt^  all  these  remedies.  Bromide 
acne  is  to  be  treated  bv^arsenic  and  hot  baths.  When  bromide 
causes  delirium,  as  it  may.  it  is  to  be  avoided, 

L.  f',.'^o{aM<x*«^   coA^U---^   ^' Chore  \. 

Qiorea,  or  St.  Mtus  Dance,  is  a  functional  neurosis  char- 
acterized by  sudden  quick  twitching  of  the  muscles. 

.  Etiology. — It  follows  rheumatism  in  30  per  cent,  of  the 
cases.  It  is  preceded  or  attended  by  endocarditis  and  valvu- 
lar disease  in  25  per  cent,  of  the  eases.     It  follows  mental  shocks 


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DISEASES    OF   THE    NERVOUS    SYSTEM.  «9 

in  40  per  cent,  of  the  cases.  It  is  often  attended  by  anaemia. 
It  occurs  in  the  spring  time  after  the  house  confinement  of 
winter.  It  is  more  common  among  the  poorly  nourished.  It 
is  a  disease  of  childhood,  but  adults  occasionally  are  affected. 

Symptoms. — The  twitching  may  be  unilateral  or  bilateral. 
It  may  aflfect  the  face  chiefly,  or  this  may  escape.  It  leads  to 
grimaces  and  diflficulty  of  talking.  It  may  be  so  intense  as  to 
necessitate  care  in  bed.  Usually  it  is  of  slight  degree.  It  may 
cause  apparent  ataxia  and  weakness  in  the  muscles  affected,  but 
is  not  followed  by  paralysis.  Heart  murmurs  are  found  in  many 
cases,  sometimes  anaemic  and  transient,  often  organic.  Anaemia 
is  often  present.  The  child  is  often  very  irritable  and  fretful. 
The  course  of  the  case  is  slow,  from  three  to  six  months.  Re- 
lapses are  very  frequent. 

Prognosis  is  good  for  recovery,  but  bad  for  recurrence. 

Treatment. — Arsenic  gradually  increased  to  point  of  tol- 
erance ;  antipyrin  or  §xalgin  in  moderate  dose  according  to  age. 


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